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. Claims 1-20, of record 12/27/2023, are pending and subject to prosecution. Priority The instant claims have a priority date of 12/27/2023. Claim Objections Claims 7- 9 and 18 are objected to because of the following informalities: In line 2 of claims 7-8, the article “an” should be inserted in front of “endogenous”. In line 2 of claim 9, “the steps of,” should be deleted. In lines 4-5 of claim 18, the word “step” should be deleted. Appropriate correction is required. Claim Rejections - 35 USC § 112 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 20 is 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. Claim 20 recites the limitation "the erythrocyte membrane" in line 1-2. There is insufficient antecedent basis for this limitation in the claim. Claim Rejections - 35 USC § 103 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 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action: A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made. This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention. Claim s 1-3 are rejected under 35 U.S.C. 103 as being unpatentable over Auffray et al. ( Blood , 2001) in view of Hsu et al. ( Blood , 2009) , evidenced by NCBI (Webpage capture, 2009) . Regarding claims 1-3: Auffray et al. teach transgenic mice expressing a human glycophorin gene (See Abstract). A BAC clone encoding glycophorin A was microinjected into fertilized mouse eggs, and a transgenic line was generated from the founder mouse expressing the highest level of glycophorin A (See page 2873, col. 1, full ¶ 1). Auffray et al. do not teach the transgenic mice as expressing a glycophorin variant. Hsu et al. teach an expression vector encoding the glycophorin variant GP.Mur (which reads on “Miltenberger blood group antigen subtype III ” ) , a hybrid of glycophorins A and B, in order to examine its structural and functional impact (See page 1919, col. 2, full ¶ 1 and page 1921, col. 1, ¶ 1). T he sequence of GP. M ur compris es a sequence identical to the sequence of instant SEQ ID NO 2 (See page 1921, col. 1, ¶1; NCBI Accession No. EU338225.1 ; and alignment below (first 120 nt displayed )). The translated sequence is identical to instant SEQ ID NO 1 (See alignment below (first 120 aa displayed)). It would have been obvious to one having ordinary skill in the art prior to the effective filing date of the claimed invention to modify the method of Auffray et al. to comprise the glycophorin gene taught by Hsu et al. One would have been motivated to make this modification because Auffray et al. teach that a mouse model can provide insights for the relationships between human glycophorin and other red cell membrane proteins in a native environment (See page 2875, col. 2, full ¶ 2 and page 2877, col. 1, full ¶ 3 and col. 2, ¶ 1) . There would be a reasonable expectation of success in making this modification because Auffray et al. demonstrate that that mice expressing a human glycophorin gene can be generated (See fig. 2-3 ). Claims 1-4 are rejected under 35 U.S.C. 103 as being unpatentable over Auffray et al. (Blood, 2001) in view of Hsu et al. (Blood, 2009) , evidenced by NCBI (Webpage capture, 2009), further in view of Lukaszewicz et al. ( WO 2016144642 A1 ) . The teachings of Auffray et al. , Hsu et al. , and NCBI are set forth in the rejection above and are incorporated herein in their entirety. Regarding claim 4: Following the discussion of claims 1-3, Auffray et al. , modified by Hsu et al. , evidenced by NCBI, render obvious the generation of a mouse expressing a mutated glycophorin transgene but do not teach the transgene as comprising an IRES. Lukaszewicz et al. teach methods of genetically engineering cells for malaria research (See Abstract). Exogenous expression of genes such as glycophorin A can be mediated from an IRES (which reads on “gene that is linked to the 3’ end of the IRES”) (See Abstract and ¶ 0075). It would have been obvious to one having ordinary skill in the art prior to the effective filing date of the claimed invention to modify the method of Auffray et al. , modified by Hsu et al. , evidenced by NCBI, to comprise a G P .Mur transgene with an IRES. One would be motivated to make this modification because Lukaszewicz et al. teach that a glycophorin transgene can be expressed from an IRES (See Abstract and ¶ 0075). There would be a reasonable expectation of success in doing so because an IRES could be readily inserted in front of a G P .Mur coding sequence. Claims 1-3 and 7-8 are rejected under 35 U.S.C. 103 as being unpatentable over Auffray et al. (Blood, 2001) in view of Hsu et al. (Blood, 2009), evidenced by NCBI (Webpage capture, 2009), further in view of Colman et al. (US 20020012660 A1). The teachings of Auffray et al. , Hsu et al. , and NCBI are set forth in the rejection above and are incorporated herein in their entirety. Regarding claims 7-8: Following the discussion of claims 1-3, Auffray et al. , modified by Hsu et al. , evidenced by NCBI, render obvious the generation of a mouse expressing a mutated glycophorin transgene but do not teach insertion of the transgene into the endogenous glycophorin A gene. Colman et al. teach methods for preparing genetically modified somatic cells (See Abstract). A transgene can be placed under the control of the endogenous promoter without disturbing the expression of the endogenous gene by inserting the transgene within the 3’ UTR (See ¶ 0201). Colman et al. teach that the genetic material of a somatic cell can be edited and then transferred to a fertilized zygote or two-cell embryo (which reads on “introducing the transgene into endogenous GYPA gene of a zygote or embryo”), and that the transfer can involve the same species, which can be a mouse (See ¶ 0027, 0030-0031, and 0043). Embryos can be transferred to a recipient animal for growing to term (See ¶ 0107). It would have been obvious to one having ordinary skill in the art prior to the effective filing date of the claimed invention to modify the method of Auffray et al. , modified by Hsu et al. , evidenced by NCBI, to comprise insertion of the GP.Mur transgene into the 3’ UTR of the glycophorin A gene. One would be motivated to make this modification because Colman et al. teach that it enables transgene expression from an endogenous promoter without disturbing en d ogenous gene expression (See ¶ 0201), and such a modification could be readily performed. It also would have been obvious to transfer the edited gene from a somatic cell to a zygote or embryo , which could then be implanted into a recipient mouse. One would also be m o tivate d to make this modification because Colman et al. teach that this approach enables the ability to carry out one or more genetic modifications in a single animal and the production of multiple cloned animals (See ¶ 0007-0013) . Claims 1- 3, 18, and 20 are rejected under 35 U.S.C. 103 as being unpatentable over Auffray et al. (Blood, 2001) in view of Hsu et al. (Blood, 2009) , evidenced by NCBI (Webpage capture, 2009), further in view of Chen et al. (Journal of the Formosan Medical Association, 2022) and Vrankova et al. (Journal of Hypertension 2009). The teachings of Auffray et al. , Hsu et al. , and NCBI are set forth in the rejection above and are incorporated herein in their entirety. Regarding claim 4: Following the discussion of claims 1-3, Auffray et al. , modified by Hsu et al. , evidenced by NCBI, render obvious the generation of a mouse expressing a mutated glycophorin transgene but do not teach its use for identifying hypertension drugs. Chen et al. teach that the GP.Mur phenotype is associated with increased blood pressure in adult human subjects (which reads on “the subject has the Mi.III antigen expressed on the erythrocyte membrane thereof”) (See Abstract). Vrankova et al. teach the use of a rodent model of hypertension for comparing the effects of two drugs (See Abstract ). Spontaneously hypertensive rats were treated with captopril and/or indapamide, and blood pressure was monitored over six weeks (See page S43, col. 1, ¶1-2 ). Each drug lowered systolic blood pressure compared to an untreated control, and the combined treatment demonstrated a greater effect (See fig. 1A). It would have been obvious to one having ordinary skill in the art prior to the effective filing date of the claimed invention to modify the method of Auffray et al. , modified by Hsu et al. , evidenced by NCBI, to comprise testing blood pressure drugs with the transgenic mice. One would be motivated to make this modification because Chen et al. teach that GP.Mur is associated with increased blood pressure (See Abstract) and because Vrankova et al. teach that a rodent model of hypertension can be used to evaluate drug treatments such as captopril (See Abstract). There would be a reasonable expectation of success in making this modification because a mouse expressing GP.Mur could be readily used for assessing the effects of hypertension drugs. Allowable Subject Matter Claims 5-6 and 9-17 are objected to as being dependent upon a rejected base claim, but would be allowable if rewritten in independent form including all of the limitations of the base claim and any intervening claims. The following is a statement of reasons for the indication of allowable subject matter: Instant SEQ ID NO s 3- 4 appear to be free of the prior art. Conclusion Any inquiry concerning this communication or earlier communications from the examiner should be directed to FILLIN "Examiner name" \* MERGEFORMAT JENNIFER S SPENCE , whose telephone number is FILLIN "Phone number" \* MERGEFORMAT 571-272-8590 . The examiner can normally be reached FILLIN "Work Schedule?" \* MERGEFORMAT M-F 8:30-5:30 . Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. 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