DETAILED ACTION Notice of Pre-AIA or AIA Status The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA. Power of Attorney It is noted that a Power of Attorney is not on record for the instant application. The Applicant is encouraged to file a Power of Attorney in the event that the Examiner needs to communicate with an authorized representative for the Applicant during the prosecution of the case. Information Disclosure Statement Applicants are kindly reminded of their duty to disclose pursuant to 37 C.F.R. 1.56 which encompasses the citation of references material to patentability of which Applicants are aware, such as references that may have been cited in the International Search Report of the parent application o r cited in the specification. Claim Status Claims 107-120 are pending and under examination in the instant office action. Claim Objections Claim FILLIN "Enter claim indentification information" \* MERGEFORMAT 107 is objected to because of the following informalities: FILLIN "Enter appropriate explanation" \* MERGEFORMAT claim 107 recites a population of engineered NK cells, but in line 2 part a) refers to "the engineered NK cell is". The examiner request that the claim be amended for consistency of the plurals such that part a) reads "the engineered NK cells are" in line 2 . Claim 1 10 is objected to because of the following informalities: FILLIN "Enter appropriate explanation" \* MERGEFORMAT claim 1 10 recites a n antigen target referred to only by the greek letter "κ". The examiner request that the full name of the antigen read in the claim, for example "Kappa light chain ( κ )". Claims 109 and 111 are objected to for the recitation of “hnCD16”. The examiner requests the first instance be amended to clarify what “ hn ” stands for in the abbreviation. Appropriate correction is required. Claim Interpretation The instant claims are broadly directed towards a population of engineered NK cells wherein the engineered NK cell is derived from an isolated stem cell or an induced stem cell. Regarding the term “a population of engineered NK cells”, the instant specification defines “engineered” with respect to a polypeptide and polynucleotide as “having a heterologous amino acid sequence or an altered amino acid sequence as a result of the application of genetic engineering techniques to nucleic acids which encode the polypeptide molecule, as well as cells or organisms which express the polypeptide molecule” [0056] and “having a heterologous nucleic acid sequence or an altered nucleic acid sequence as a result of the application of genetic engineering techniques” [0056] . Although these are not closed definitions, these are consistent with the definition an artisan would give an “engineered NK cell” (For example, see Muldoon, Joseph J., et al. "Building with intent: technologies and principles for engineering mammalian cell-based therapies to sense and respond." Current opinion in biomedical engineering 4 (2017): 127-133 ). Therefore, as described in the specification and the art, an “engineered NK cell” will be interpreted as an NK cell comprising an engineered polypeptide or an engineered nucleotide having a heterologous amino acid sequence or an altered amino acid sequence as a result of the application of genetic engineering techniques to nucleic acids which encode the polypeptide molecule or having a heterologous nucleic acid sequence or an altered nucleic acid sequence as a result of the application of genetic engineering techniques . Regarding the recitation of “the engineered NK cell is derived from an isolated stem cell or an induced stem cell”, the phrase “is derived” refers to the process by which the NK cell is made. MPEP 2113 teaches that product-by-process claims are not limited to the manipulations of the recited steps, only the structure implied by the steps. As the purpose of differentiating NK cells in vitro from isolated stem cells is to produce NK cells that are substantially the same as NK cells (which are derived from non-isolated stem cells)(evidenced by, for example, Bock AM, et. al . Development, expansion, and in vivo monitoring of human NK cells from human embryonic stem cells ( hESCs ) and and induced pluripotent stem cells (iPSCs). J Vis Exp. 2013 Apr 23;(74):e50337. doi : 10.3791/50337 ), there is no additional structure required of the NK cell by the recitation that it is derived from an isolated stem cell or induced stem cell. Claim Rejections - 35 USC § 112(b) The following is a quotation of 35 U.S.C. 112(b): (b ) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention. The following is a quotation of 35 U.S.C. 112 (pre-AIA), second paragraph: The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the appl icant regards as his invention. Claim s 108-111 and 117-120 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention. Regarding c laims 108, 109, 110, 111, 117, 118, 119, and 120 , the phrase “preferably” renders the claim indefinite because it is unclear whether the limitations following the phrase are part of the claimed invention. See MPEP §2173.05(d). For the purposes of expedited prosecution, the claims will be read without any limitations that follow the “preferably”. Regarding claim 112, the claim is directed to where the engineered NK cell further comprises a hypo-immunity regulator polypeptide or the nucleotide coding sequence thereof, or modified expression of an endogenous hypo-immunity regulator polypeptide. This is unclear because claim 112 is ultimately dependent on claim 107, which recites the NK cell comprises a heterologous polypeptide or the nucleotide coding sequence thereof, or reduced expression of an endogenous immune regulating polypeptide or modification of the nucleotide coding sequence of the endogenous immune regulating polypeptide. This is unclear because the “further comprising” language does not make it clear whether the hypo-immunity regulator polypeptide of claim 112 may be the same as the heterologous polypeptide of claim 107 or must be a different polypeptide, or whether the modified expression of an endogenous hypo-immunity regulator polypeptide of claim 112 may be the same as the reduced expression of an endogenous immune regulating polypeptide of claim 107 or must be a different reduced expression or modification. For the purposes of expedited prosecution, the claim will be interpreted such that “further comprises” is in addition to limitations ( i )-(iii) of claim 111, and therefore the hypo-immunity regulator polypeptide or the endogenous hypo-immunity regulator polypeptide may be the same as the heterologous polypeptide of claim 107 or the endogenous immune regulating polypeptide of claim 107. A broad range or limitation together with a narrow range or limitation that falls within the broad range or limitation (in the same claim) may be considered indefinite if the resulting claim does not clearly set forth the metes and bounds of the patent protection desired. See MPEP § 2173.05(c). In the present instance, claim 117 recites the broad recitation “at least about 5%” (lines 3 and 16) , and “at least about 0.1-fold” (line 10) , and the claim also recites “at least about 30%” (line 4), “at least about 5-fold”, and “at least about 50%” (line 16) which is the narrower statement of the range/limitation. The claim(s) are considered indefinite because there is a question or doubt as to whether the feature introduced by such narrower language is (a) merely exemplary of the remainder of the claim, and therefore not required, or (b) a required feature of the claims. Additionally, the phrase “at least” is a narrower limitation followed by “about”, which is a broader limitation, and so it is unclear whether there is a minimum or a range being claimed. The examiner suggests amending the claims to recite “at least” rather than “at least about”. Claim 117 is rejected for recitation of intended result/effect without conferring some structural, material, or manipulative difference on the scope of the claim. Claim 117 recites, wherein “a persistence level of the population of engineered NK cells in an environment that is substantially free of an exogenous interleukin-2 is at least about 5% […] or at least about 30% greater than a control persistence level of a comparable population of NK cells in a control environment comprising the exogenous IL-2”; “the population of engineered NK cells exhibits enhanced resistance against immune rejection by at least about 5% […] or at least about 50% as compared to that of a control population of NK cells lacking the at least one heterologous hypo-immunity regulator polypeptide”. It is unclear what compositions are encompassed by the functional language because the “comparable population of NK cells” in part ( i ) is unclear. What would make an NK cell population comparable? Additionally, part (iii) recites at least about a 5% increase or at least about a 50% increase in “persistence level”. This is unclear because it is uncertain what “persistence level” is defined as; would it require 5% more living cells at a particular point? Or 5% greater amount of time with a particular number of cells? 5% greater levels of cells within a tumor at a particular time point? Additionally, all of these limitations are related to function with no additional specified structure added to the claim. MPEP 2173.05(g) states: “the use of functional language in a claim may fail ‘to provide a clear-cut indication of the scope of the subject matter embraced by the claim' and thus be indefinite.” It further states: “Examiners should consider the following factors when examining claims that contain functional language to determine whether the language is ambiguous: (1) whether there is a clear cut indication of the scope of the subject matter covered by the claim; (2) whether the language sets forth well-defined boundaries of the invention or only states a problem solved or a result obtained; and (3) whether one of ordinary skill in the art would know from the claim terms what structure or steps are encompassed by the claim” (emphasis added). Since the claim fail to meet all (3) criteria set forth in MPEP 2173.05(g) , claim 117 is rejected. Claim Rejections - 35 USC § 112(a) - Written Description The following is a quotation of the first paragraph of 35 U.S.C. 112(a): (a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention. The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112: The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention. Claims 107-120 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention. Regarding claim 107 , the claims recite an engineered NK cell population derived from an isolated stem cell or an induced stem cell wherein an engineered NK cell of the population comprises any generic heterologous polypeptide or the nucleotide coding sequence thereof or a reduced expression of any endogenous immune regulating polypeptide or any generic modification of the nucleotide coding sequence of the endogenous immune regulating polypeptide, wherein the immune regulating polypeptide is claimed only by function or enhanced or introduced expression of NKG2C; the remaining limitations of the claim are recited as optional. This scope is so broad as to encompass nearly any stem-cell derived NK cell with no additional structure. Scope of the claimed genus C laim 107 is broadly directed towards a genus of engineered NK cell population s derived from an isolated stem cell or an induced stem cell wherein an engineered NK cell of the population comprises any generic heterologous polypeptide or the nucleotide coding sequence thereof or a reduced expression of any endogenous immune regulating polypeptide or any generic modification of the nucleotide coding sequence of the endogenous immune regulating polypeptide, wherein the immune regulating polypeptide is claimed only by function or enhanced or introduced expression of NKG2C; the remaining limitations of the claim are recited as optional. Regarding the reduced or enhanced expression, these are not closed defin itions in the specification and , even if the definition were closed, there are no requirements in the specification for the degree of reduction or enhancement (“ The term "enhanced expression,""increased expression," or "upregulated expression" generally refers to production of a moiety of interest (e.g., a polynucleotide or a polypeptide) to a level that is above a normal level of expression of the moiety of interest in a host strain (e.g., a host cell) ” [0073], “ The term "reduced expression,""decreased expression," or "downregulated expression" generally refers to a production of a moiety of interest (e.g., a polynucleotide or a polypeptide) to a level that is below a normal level of expression of the moiety of interest in a host strain (e.g., a host cell) ” [0075]) . There is also no requirement for any link between the limitation for the cell to be engineered and the reduction or enhancement. For example, the scope of the claim 107 includes an NK cell that is engineered to express a chimeric antigen receptor (CAR) that then upon exposure to any environmental stimulus decreases expression of any immune regulating gene. Regarding modification, there are examples of modification in the specification but there is no further definition. The claims re cite modification to the nucleotide coding sequence, but there is no requirement that the modification result in any difference to the peptide sequence. As described in the 112(b) section above, claims 108-110 are directed towards further limiting optional limitation of claim 107, and are therefore also optional. Claim 111 is directed towards the engineered NK cell population wherein an engineered NK cell of the population comprises a CAR specifically recognizing an antigen from a group; a heterologous CD16 variant for enhanced CD16 signaling; and a heterologous IL-15. Claim 112 is directed towards the NK cell of population of claim 111 wherein the NK cells further comprises a hypo-immunity regulator peptide or the nucleotide coding sequence thereof, or modified expression of an endogenous hypo-immunity regulator polypeptide for enhanced resistance against immune rejection, wherein a hypo-immunity regulator peptide is defined only by function. Regarding the phrase “hypo-immunity regulator”, the instant specification says that the term “generally refers to a polypeptide construct in a cell, wherein either enhanced expression or reduced expression of the hypo-immunity regulator in the cell can help the cell to reduce or avoid immune response from a host’s body upon administration to the host’s body ([0068]). Further, the hypo-immunity regulator polypeptide or the nucleotide sequence thereof has no requirement to be a heterologous hypo-immunity regulator polypeptide; therefore, the scope of the claim includes any engineered NK cell meeting the limitations of claim 111 because every NK cell would be expected to express self HLA (which is expressed on all nucleated cells as evidenced by Bettens F, et al. (2022) Regulation of HLA class I expression by non-coding gene variations. PLoS Genet 18(6): e1010212. https://doi.org/10.1371/journal.pgen.1010212 ) and therefore would comprise a hypo-immunity regulator polypeptide and the nucleotide coding sequence thereof. Claim 113 is directed towards wherein the hypo-immunity regulator polypeptide for enhanced resistance against immune rejection comprises one or more members selected from a group or the modified expression of the endogenous hypo-immunity regulator polypeptide is selected from one or more members of a group. Claim 114 is directed towards the population wherein the enhanced or introduced expression or the reduced expression or activity is from a narrower group; claim 115 recites wherein the enhanced or introduced expression is HLA-E and HLA-G and reduced expression of B2M and CIITA. Claim 116 recites the population of claim 115 wherein the NK cell population further comprises enhanced or introduced expression of PDL1 and/or CD47. Claim 117 recites the population of claim 107 wherein the population exhibits particular characteristics or intended effects of the genetic engineering (e.g. a persistence level in an environment substantially free of exogenous IL-2 is at least about 5% greater than a control persistence level of a comparable population of NK cells in a control environment comprising the exogenous IL-2. Claim 118 recites a composition comprising the population of claim 107. Claim s 119 recite a method for treating any generic disease in a subject comprising administering the population of claim 107 . C laim 120 recites a method for treating any generic disease in a subject by administering the composition of claim 118 (which is a composition comprising the population of claim 107 as described above). State of the Relevant Art Engineered NK cells are known in the art. The earliest examples are related to the engineering of immortalized NK cell lines. For example, Boissel et. al. teaches transfection of NK-92 cells with an mRNA for a CD19 specific CAR directed NK-cell mediated killing of CLL cells ( Boissel , Laurent, et al. "Transfection with mRNA for CD19 specific chimeric antigen receptor restores NK cell mediated killing of CLL cells." Leukemia research 33.9 (2009): 1255-1259 ). Sahm , Christiane, et. al . "Expression of IL-15 in NK cells results in rapid enrichment and selective cytotoxicity of gene-modified effectors that carry a tumor-specific antigen receptor." Cancer Immunology, Immunotherapy 61.9 (2012): 1451-146 1 teaches NK-92 cells engineered to express both human IL-15 and a CAR targeting EpCAM . Methods to genetically modify stem cells and then subsequently differentiate into NK cells are also taught in the art. Eguizabal et. al. teaches “ Apart from that, with continued advances in the stem cell field, it is likely that hPSC -derived NK cells will relatively soon be able to be efficiently derived on a patient-specific basis. Actually, hESC and hiPSC -derived NK cells express activating and inhibitory receptors similar to NK cells isolated from adult peripheral blood (100, 104, 108, 130). The hESC -derived NK cells are also highly efficient at direct cell-mediated cytotoxicity and ADCC, as well as cytokine (IFN-γ) production. And importantly, stromal cells-free protocols have successfully been described (100, 130). It is clear that hiPSC -derived NK cells provide a genetically manageable system to study human NK-cell development and function ” ( Eguizabal , Cristina, et al. "Natural killer cells for cancer immunotherapy: pluripotent stem cells-derived NK cells as an immunotherapeutic perspective." Frontiers in immunology 5 (2014): 439 ). Morgan, Michael A., et al. "Use of cell and genome modification technologies to generate improved “off-the-shelf” CAR T and CAR NK cells." Frontiers in immunology 11 (2020): 1965 teaches NK CAR therapies have been made derived from cord blood (“NK cell sources” section p. 4) and from iPSCs (“iPSC and other cell sources” section, p. 5), including that one advantage of iPSC-derived CAR NK cells is “their enormous proliferative capacities as well as the relative ease of genomic modification” (p. 5 right column ¶1). Regarding decreased expression of an endogenous immune regulating gene, e ngineering of HSCs from which NK cells are produced is also known in the art. For example, Xu, Lei, et al. "CRISPR/Cas9-mediated CCR5 ablation in human hematopoietic stem/progenitor cells confers HIV-1 resistance in vivo." Molecular Therapy 25.8 (2017): 1782-1789 teaches knockout of the immune-regulating CCR5 gene in HSCs for the treatment of HIV, after which NK cells are reconstituted (See Graphical Abstract, Abstract, Fig. 2B). Additionally, environmental inputs are known to change gene expression of immune-regulating genes in NK cells. For example, Mori, S., et. al. “ Differential regulation of human NK cell-associated gene expression following activation by IL-2, IFN-alpha and PMA/ionomycin.". International Journal of Oncology 12.5 (1998): 1165-1235 teaches that CD16 expression decreased on NK cells in response to activating stimulus of PMA/Ionomycin (Fig. 3 and Table III). Thus, the art teaches that enhancement or reduction of gene expression relative to a normal is a vast genus that includes changes that are within the scope of endogenous gene regulation. Regarding IL-15, claim 108 recites a heterologous fragment of IL-15. While IL-15 is known in the art, there is no further definition of the IL-15 fragment that would limit how small the fragment may be. For example, Chertova , Elena, et al. "Characterization and favorable in vivo properties of heterodimeric soluble IL-15· IL-15Rα cytokine compared to IL-15 monomer." Journal of Biological Chemistry 288.25 (2013): 18093-18103 teaches a soluble heterodimer comprising IL-15 and soluble IL-15 receptor ɑ. However, there are no additional fragments of IL-15 of record that comprise less than an IL-15 polypeptide. Regarding heterologous CD16 variants (see claim 109 and claim 111), some variants are known in the art. For example, Zhu, Huang, et al. "Pluripotent stem cell–derived NK cells with high-affinity noncleavable CD16a mediate improved antitumor activity." Blood, The Journal of the American Society of Hematology 135.6 (2020): 399-410 teaches a high-affinity non-cleavable CD16 variant comprising 158V mutation and an S197P mutation which increased NK cell killing when combined with monoclonal antibodies . However, an artisan would not be able to at once envision any and all CD16 variants, including those yet to be invented. Regarding a hypo-immunity regulator polypeptide, some of these are described in the art; however, this is a genus defined only by function. This genus also includes proteins wherein increased expression decreases the host immune response or wherein decrease expression decreases the host immune response (see scope of the claims section above). For example, Gornalusse , Germán G., et al. "HLA-E-expressing pluripotent stem cells escape allogeneic responses and lysis by NK cells." Nature biotechnology 35.8 (2017): 765-772 teaches that ‘missing-self’ of lysis by host NK cells can be prevented by forced expression of minimally polymorphic HLA-E molecules. Additionally, Deuse , Tobias, et al. "Hypoimmunogenic derivatives of induced pluripotent stem cells evade immune rejection in fully immunocompetent allogeneic recipients." Nature biotechnology 37.3 (2019): 252-258 teaches knockout of B2M and CIITA along with heterologous expression of CD47 for reducing immunogenicity of allogeneic cells (Abstract) . Additionally, claim 112 is drafted such that the NK cell of claim 111 further comprises a hypo-immunity regulator polypeptide. As described above, this would include basically any NK cell because nucleated cells express class I HLA, which is a hypo-immunity regulator polypeptide in the context of a syngeneic recipient (see Scope of the claims section above). This also applies to other known hypo-immunity regulators. For example, PD-L1 is known to be expressed in some populations of NK cells based on different environmental contexts such as in response to a tumor ( Iraolagoitia , Ximena L. Raffo , et al. "NK cells restrain spontaneous antitumor CD8+ T cell priming through PD-1/PD-L1 interactions with dendritic cells." The Journal of Immunology 197.3 (2016): 953-961 ). There are no structural similarities between these peptides that would relate to their common functions that would allow an artisan to determine a priori which peptides or genes are hypo-immunity regulator polypeptides outside of those which are already known to increase immune tolerance. Further, upstream regulators of known hypo-immunity regulator polypeptides would also fall under the definition of hypo-immunity regulator polypeptides, and would therefore fall within the scope of the claims. An artisan would not understand from the state of the art or the instant specification the applicant to be in possession of any engineered NK cell as described comprising any reduction or any enhancement of the hypo-immunity regulator polypeptides as claimed. Summary of Species disclosed in the original specification The instant specification discloses NK-92 cells expressing CD16 (Fig. 1) or a CAR (Fig. 2) as well as NK-92 cells expressing IL15 (Fig. 3B). The instant specification teaches embryonic stem cell (ESC) derived NK cells comprising B2M and hCIITA single knockouts (Fig. 12B-C); a B2M CIITA double knockout (Edit-4, see Fig. 18); and six additional edits with combinations of B2M and CIITA knockout with knock-in expression of combinations of or all of PD-L1, PD-L2, TGFβ, HLA-E, HLA-G, CD47, IL-10, CCL-21, CD46, CD55, and CD59 and additional knockdown of MICA, MICB, or ULBP1 (Fig. 18 , See [0454-0492] ). These edits are prophetically combined with the CAR, hnCD16, and IL-15 expression ( e.g. [0516]). Regarding IL-15, the instant specification describes heterologous secretory IL-15 and/or membrane-bound IL-15, such as IL-15-IL-15 receptor fusion ([0181], [0189]). The specification does not disclose any particular fragments of IL-15 or what the minimal fragment required for activity would be. Regarding heterologous CD16 variants, the instant specification discloses S197P and the non-cleavable variant and F176V as the high affinity variant ([0107-0108]). The specification also prophetically discloses variants comprising a portion of CD16 and the ectodomain of a different cell surface protein (e.g. CD64) ([0107-0108] , Table 1 p. 70 ) . Regarding hypo-immunity regulator polypeptides, the instant specification prophetically discloses a long list of genes /peptides: ICAM1 , B2M, CIITA, TAP1, TAP2, tapasin , NLRC5, RFXANK, RFX5, RFXAP, CD80, CD86, ICOSL, CD40L, MICA, MICB, ULBP1, HLA-Et. al., CD47, CD113, PDL1, PDL2, A2AR, HLA-G, TGF-beta, CCL21, IL-10, CD46, CD55, CD59 ([0171-0179] , [0199], [0212], [0213], Table 6 ) . All of the reduced expression disclosed are complete gene-edited knockouts. All of the enhanced expression are heterologous gene knock-in or overexpression. There is no reduction of gene expression through an upstream regulator or an indirect means. There are no reduced expression via RNA interference or non-genomic engineering methods of reducing expression, such as cell sorting for low expression. One of skill in the art would reasonably conclude that applicant was not in possession of the required genus of populations of NK cells comprising any heterologous polypeptide or any reduced expression of an endogenous immune regulating polypeptide, or any enhanced or introduced expression of NKG2C; or any chimeric polypeptide receptor comprising an antigen binding moiety binding to any target with no additional required CAR structure; or any and all generic heterologous IL-15 or any fragment thereof; or any and all variants for enhanced CD16 signaling; NK cells comprising a combination of the above elements an comprising any hypo-immunity regulator polypeptide. Summary A genus of species is not present in the instant specification or prior art that would demonstrate a structure/activity relationship would be known for the instant populations of NK cells comprising any polypeptide, or any reduction in any immune-regulating gene, or for the entire scope of the individual peptides and variants of the dependent claims (e.g. CD16, IL-15, hypo-immunity regulators) for any cell comprising the peptides or any reduced or enhanced expression . There is a lack of an appropriate number of species of each claimed genus that are essential for each claimed function (e.g. immune regulating, hypo-immunity, fragments of IL-15) . One of skill in the art would reasonably conclude that the applicant was not in possession of the genus populations of engineered NK cells of claim 107 as described . Regarding claims 108-120 the claims are ultimately dependent on the rejected claim 107 without sufficiently narrowing the claimed subject matter as desc r ibed in the rejection above and thus are also rejected. Claim Rejections - 35 USC § 112(a) - Scope of Enablement Claims FILLIN "Enter claim identification information" \* MERGEFORMAT 119 and 120 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA), first paragraph, because the specification, while being enabling for FILLIN "Identify claimed subject matter for which the specification is enabling" \* MERGEFORMAT A method for treating a cancer or tumor expressing a target antigen selected from the group consisting of CD33, CD19, and BCMA comprising administering a therapeutically effective amount of the population of claim 111, wherein the cancer or tumor expresses the same target antigen that is specifically recognized by the CAR ; wherein the heterologous CD16 variant comprises the CD16 variant encoded by the amino acid sequence SEQ ID NO: 1; wherein the heterologous hIL-15 is an IL-15-IL-15Rɑ comprising SEQ ID NO: 13 or SEQ ID NO: 14. does not reasonably provide enablement for FILLIN "Identify aspects of claims for which the specification is not enabling" \* MERGEFORMAT a method of treating any generic in any subject comprising administering the population of claim 107 or the composition of claim 118 to the subject . The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to FILLIN "Enter --make-- or --use-- or --make and use--" \* MERGEFORMAT perform the method of the invention commensurate in scope with these claims. In order to determine compliance with the enablement requirement of 35 U.S.C. 112(a), the Federal Circuit developed a framework of factors in In re Wands , 858 F.2d 731, 737, 8 USPQ2d 1400, 1404 (Fed. Cir. 1988), referred to as the Wands factors to assess whether any necessary experimentation required by the specification is "reasonable" or is "undue." Consistent with Amgen Inc. et al. v. Sanofi et al., 598 U.S. 594, 2023 USPQ2d 602 (2023), the Wands factors continue to provide a framework for assessing enablement in a utility application or patent, regardless of technology area. In In re Wands, 8 USPQ2d 1400 (Fed. Cir., 1988) eight factors included for determining enablement: (A) The breadth of the claims; (B) The nature of the invention; (C) The state of the prior art; (D) The level of one of ordinary skill; (E) The level of predictability in the art; (F) The amount of direction provided by the inventor; (G) The existence of working examples; and (H) The quantity of experimentation needed to make or use the invention based on the content of the disclosure. The following is an analysis of these factors in relationship to this application. Scope of the claimed genus and nature of the invention Instant claims 119 and 120 are directed towards a method of treating a generic disease in a subject comprising administering the population of NK cells of claim 107 (claim 119) or the composition of claim 118 (a composition comprising the NK cells of claim 107). As described in the written description rejection above, Claim 107 is broadly directed towards a genus of engineered NK cell populations derived from an isolated stem cell or an induced stem cell wherein an engineered NK cell of the population comprises any generic heterologous polypeptide or the nucleotide coding sequence thereof or a reduced expression of any endogenous immune regulating polypeptide or any generic modification of the nucleotide coding sequence of the endogenous immune regulating polypeptide, wherein the immune regulating polypeptide is claimed only by function or enhanced or introduced expression of NKG2C; the remaining limitations of the claim are recited as optional. Regarding the reduced or enhanced expression, these are not closed definitions in the specification and, even if the definition were closed, there are no requirements in the specification for the degree of reduction or enhancement (“The term "enhanced expression,""increased expression," or "upregulated expression" generally refers to production of a moiety of interest (e.g., a polynucleotide or a polypeptide) to a level that is above a normal level of expression of the moiety of interest in a host strain (e.g., a host cell)” [0073], “The term "reduced expression,""decreased expression," or "downregulated expression" generally refers to a production of a moiety of interest (e.g., a polynucleotide or a polypeptide) to a level that is below a normal level of expression of the moiety of interest in a host strain (e.g., a host cell)” [0075]). There is also no requirement for any link between the limitation for the cell to be engineered and the reduction or enhancement. For example, the scope of the claim 107 includes an NK cell that is engineered to express a chimeric antigen receptor (CAR) that then upon exposure to any environmental stimulus decreases expression of any immune regulating gene. Regarding modification, there are examples of modification in the specification but there is no further definition. The claims recite modification to the nucleotide coding sequence, but there is no requirement that the modification result in any difference to the peptide sequence. State of the relevant art; level of one of ordinary kill; and the level of predictability in the art Regarding methods of treatment of diseases with NK cells, methods of treating cancer by administering engineered NK cells are known in the art. CAR-NK cell therapy has advanced into clinical applications, for instance Xiao, Lin, et al. "Adoptive transfer of NKG2D CAR mRNA-engineered natural killer cells in colorectal cancer patients." Molecular Therapy 27.6 (2019): 1114-1125 teach adoptive transfer of NKG2D CAR with a DAP12-based intracellular signaling domain for the treatment of colorectal cancer in human subjects (entire document). Genetic engineering in order to increase the performance of NK cell therapies is known in the art. The earliest examples are related to the engineering of immortalized NK cell lines. For example, Boissel et. al. teaches transfection of NK-92 cells with an mRNA for a CD19 specific CAR directed NK-cell mediated killing of CLL cells ( Boissel , Laurent, et al. "Transfection with mRNA for CD19 specific chimeric antigen receptor restores NK cell mediated killing of CLL cells." Leukemia research 33.9 (2009): 1255-1259 ). Sahm , Christiane, et. al . "Expression of IL-15 in NK cells results in rapid enrichment and selective cytotoxicity of gene-modified effectors that carry a tumor-specific antigen receptor." Cancer Immunology, Immunotherapy 61.9 (2012): 1451-146 1 teaches NK-92 cells engineered to express both human IL-15 and a CAR targeting EpCAM . Methods to genetically modify stem cells and then subsequently differentiate into NK cells are also taught in the art. Eguizabal et. al. teaches “ Apart from that, with continued advances in the stem cell field, it is likely that hPSC -derived NK cells will relatively soon be able to be efficiently derived on a patient-specific basis. Actually, hESC and hiPSC -derived NK cells express activating and inhibitory receptors similar to NK cells isolated from adult peripheral blood (100, 104, 108, 130). The hESC -derived NK cells are also highly efficient at direct cell-mediated cytotoxicity and ADCC, as well as cytokine (IFN-γ) production. And importantly, stromal cells-free protocols have successfully been described (100, 130). It is clear that hiPSC -derived NK cells provide a genetically manageable system to study human NK-cell development and function ” ( Eguizabal , Cristina, et al. "Natural killer cells for cancer immunotherapy: pluripotent stem cells-derived NK cells as an immunotherapeutic perspective." Frontiers in immunology 5 (2014): 439 ). Morgan, Michael A., et al. "Use of cell and genome modification technologies to generate improved “off-the-shelf” CAR T and CAR NK cells." Frontiers in immunology 11 (2020): 1965 teaches NK CAR therapies have been made derived from cord blood (“NK cell sources” section p. 4) and from iPSCs (“iPSC and other cell sources” section, p. 5), including that one advantage of iPSC-derived CAR NK cells is “their enormous proliferative capacities as well as the relative ease of genomic modification” (p. 5 right column ¶1). Regarding decreased expression of an endogenous immune regulating gene, engineering of HSCs from which NK cells are produced is also known in the art. For example, Xu, Lei, et al. "CRISPR/Cas9-mediated CCR5 ablation in human hematopoietic stem/progenitor cells confers HIV-1 resistance in vivo." Molecular Therapy 25.8 (2017): 1782-1789 teaches knockout of the immune-regulating CCR5 gene in HSCs for the treatment of HIV, after which NK cells are reconstituted (See Graphical Abstract, Abstract, Fig. 2B). Additionally, environmental inputs are known to change gene expression of immune-regulating genes in NK cells. For example, Mori, S., et. al. “ Differential regulation of human NK cell-associated gene expression following activation by IL-2, IFN-alpha and PMA/ionomycin.". International Journal of Oncology 12.5 (1998): 1165-1235 teaches that CD16 expression decreased on NK cells in response to activating stimulus of PMA/Ionomycin (Fig. 3 and Table III). Thus, the art teaches that enhancement or reduction of gene expression relative to a normal is a vast genus that includes changes that are within the scope of endogenous gene regulation. Regarding IL-15, claim 108 recites a heterologous fragment of IL-15. While IL-15 is known in the art, there is no further definition of the IL-15 fragment that would limit how small the fragment may be. For example, Chertova , Elena, et al. "Characterization and favorable in vivo properties of heterodimeric soluble IL-15· IL-15Rα cytokine compared to IL-15 monomer." Journal of Biological Chemistry 288.25 (2013): 18093-18103 teaches a soluble heterodimer comprising IL-15 and soluble IL-15 receptor ɑ. However, there are no additional fragments of IL-15 of record that comprise less than an IL-15 polypeptide. Regarding heterologous CD16 variants (see claim 109 and claim 111), some variants are known in the art. For example, Zhu, Huang, et al. "Pluripotent stem cell–derived NK cells with high-affinity noncleavable CD16a mediate improved antitumor activity." Blood, The Journal of the American Society of Hematology 135.6 (2020): 399-410 teaches a high-affinity non-cleavable CD16 variant comprising 158V mutation and an S197P mutation which increased NK cell killing when combined with monoclonal antibodies. However, an artisan would not be able to at once envision any and all CD16 variants, including those yet to be invented. Regarding a hypo-immunity regulator polypeptide, some of these are described in the art; however, this is a genus defined only by function. This genus also includes proteins wherein increased expression decreases the host immune response or wherein decrease expression decreases the host immune response (see scope of the claims section above). For example, Gornalusse , Germán G., et al. "HLA-E-expressing pluripotent stem cells escape allogeneic responses and lysis by NK cells." Nature biotechnology 35.8 (2017): 765-772 teaches that ‘missing-self’ of lysis by host NK cells can be prevented by forced expression of minimally polymorphic HLA-E molecules. Additionally, Deuse , Tobias, et al. "Hypoimmunogenic derivatives of induced pluripotent stem cells evade immune rejection in fully immunocompetent allogeneic recipients." Nature biotechnology 37.3 (2019): 252-258 teaches knockout of B2M and CIITA along with heterologous expression of CD47 for reducing immunogenicity of allogeneic cells (Abstract). Additionally, claim 112 is written such that the NK cell of claim 111 further comprises a hypo-immunity regulator polypeptide. As described above, this would include basically any NK cell because nucleated cells express class I HLA, which is a hypo-immunity regulator polypeptide in the context of a syngeneic recipient (see Scope of the claims section above). This also applies to other known hypo-immunity regulators. For example, PD-L1 is known to be expressed in some populations of NK cells based on different environmental contexts such as in response to a tumor ( Iraolagoitia , Ximena L. Raffo , et al. "NK cells restrain spontaneous antitumor CD8+ T cell priming through PD-1/PD-L1 interactions with dendritic cells." The Journal of Immunology 197.3 (2016): 953-961 ). There are no references of record of treating diseases other than cancer by administering a population of engineered NK cells. Summary of species disclosed in the original specification; the amount of direction provided by the inventor; existence of working examples; and the quantity of experimentation needed to make or use the invention based on the content of the disclosure Regarding methods of administering to a subject, the instant specification has one working example wherein eNK cells expressing membrane-bound IL-15, aCD19 CAR, and an unspecified CD16 variant were administered to a Nalm-6 xenograft model ([0435], Fig. 9) . The specification states “Any one of the methods disclosed herein can be utilized to treat a target cell, a target tissue, a target condition, or a target disease of a subject” [0279]. The example shows that the expansion of the cells was better than control NK cells, but there is no data provided on cancer treatment of the xenograft model. The specification further states that a disease cell can be a cancer cell, a diabetic cell, and an apoptotic cell and that exemplary diseases can include blood disorders, cancers, metabolic disorders, eye disorders, organ disorders, musculoskeletal disorders, cardiac disease, and the like [0281]. The specification discloses that particular target cells of interest are cancer cells [0289] and “a cell associated or is suspected to be associate with an autoimmune disease” [0290-0291]. The specification prophetically discloses particular genetic modifications of the NK cells with particular therapeutic indications (Table 1 p. 70-71; e.g. “CAR + IL15+ hnCD16 + TME genes + hypo-immunity genes (for re-dosing) […] Blood cancer, solid tumor”). This direction is very generalized and would not help indicate to an artisan how to treat a disease that is not a cancer, and in particular the well described treatment of administering an effector immune cell comprising a CAR, wherein the CAR specifically binds to a target antigen expressed by a cancer. The instant specification discloses NK-92 cells expressing a particular CD16 variant (Fig. 1) or a CAR (Fig. 2) as well as NK-92 cells expressing IL15 (Fig. 3B) ; in some instances, the cells were tested for cytotoxicity against cancer cell lines ([0372], [0378], [0410]-[0414]) . The instant specification teaches embryonic stem cell (ESC) derived NK cells comprising B2M and hCIITA single knockouts (Fig. 12B-C); a B2M CIITA double knockout (Edit-4, see Fig. 18); and six additional edits with combinations of B2M and CIITA knockout with knock-in expression of combinations of or all of PD-L1, PD-L2, TGFβ, HLA-E, HLA-G, CD47, IL-10, CCL-21, CD46, CD55, and CD59 and additional knockdown of MICA, MICB, or ULBP1 (Fig. 18, See [0454-0492]). These edits are prophetically combined with the CAR, hnCD16, and IL-15 expression (e.g. [0516]). Regarding IL-15, the instant specification describes heterologous secretory IL-15 and/or membrane-bound IL-15, such as IL-15-IL-15 receptor fusion ([0181], [0189]). The specification does not disclose any particular fragments of IL-15 or what the minimal fragment required for activity would be. Regarding heterologous CD16 variants, the instant specification discloses S197P and the non-cleavable variant and F176V as the high affinity variant ([0107-0108]). The specification also prophetically discloses variants comprising a portion of CD16 and the ectodomain of a different cell surface protein (e.g. CD64) ([0107-0108] , Table 1 p. 70 ) . Regarding hypo-immunity regulator polypeptides, the instant specification prophetically discloses a long list of genes/peptides: ICAM1, B2M, CIITA, TAP1, TAP2, tapasin , NLRC5, RFXANK, RFX5, RFXAP, CD80, CD86, ICOSL, CD40L, MICA, MICB, ULBP1, HLA-Et. al., CD47, CD113, PDL1, PDL2, A2AR, HLA-G, TGF-beta, CCL21, IL-10, CD46, CD55, CD59 ([0171-0179], [0199], [0212], [0213], Table 6). All of the reduced expression disclosed are complete gene-edited knockouts. All of the enhanced expression are heterologous gene knock-in or overexpression. There is no reduction of gene expression through an upstream regulator or an indirect means. There are no reduced expression via RNA interference or non-genomic engineering methods of reducing expression, such as cell sorting for low expression. Conclusion The applicant does not have enablement for a method of treating any generic disease comprising administering a population of engineered NK cells or a composition comprising the population (claims 107 and 118), wherein the NK cell comprises any heterologous polypeptide or any reduced expression of an endogenous immune regulating polypeptide or any modification of the nucleotide coding sequence of the endogenous immune regulating polypeptide, or an enhance or introduced expression of NKG2C. It would require undue experimentation to determine a suitable treatment for all generic diseases and which compositions comprising any generic heterologous polypeptide, or any reduction of immune-regulating polypeptide defined only by function, or any modification of the nucleotide coding sequence, wherein the modification is not required to result in a change to the peptide or any enhanced or introduced expression of NKG2C (which are not fully described as in the written description rejection above). Claim Rejections - 35 USC § 102 In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis ( i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status. The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action: A person shall be entitled to a patent unless – (a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale , or otherwise available to the public before the effective filing date of the claimed invention. (a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention. Claim s 107-114 and 117-1 20 are rejected under 35 U.S.C. 102 FILLIN "Insert either \“(a)(1)\” or \“(a)(2)\” or both. If paragraph (a)(2) of 35 U.S.C. 102 is applicable, use form paragraph 7.15.01.aia, 7.15.02.aia or 7.15.03.aia where applicable." \d "[ 2 ]" (a)(2) as being FILLIN "Insert either—clearly anticipated—or—anticipated—with an explanation at the end of the paragraph." \d "[ 3 ]" anticipated by FILLIN "Insert the prior art relied upon." \d "[ 4 ]" US 20210015859 to Valamehr et. al. effectively filed 8 December 2017 . Valamehr et. al. teaches methods and compositions for obtaining functionally enchanced derivative effector cells obtained from directed differentiation of engineered iPSCs (Abstract). Regarding claim 107, Valam ehr et. al. teaches a cell or a population thereof, wherein the cell is an iPSC or a derivative cell obtained from differentiating an iPSC, wherein the cell is a derivative NK cell or a derivative T cell, and the cell comprises a high affinity non-cleavable CD16, a CAR, with or without a partial or full peptide of a cell surface expressed exogenous cytokine or a receptor thereof ([0020], reads on comprises a heterologous polypeptide). The examiner notes that all of the other limitations recited in the claim are ei