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. Application Status and Election Applicant’s amendments filed February 13, 2026, amending claims 4 and 13 is acknowledged. Claims 1-17 and 20 are pending. Applicant’s election of Group I, encompassing claims 1-17 in the reply filed on February 13, 2026 is acknowledged. Because applicant did not distinctly and specifically point out the supposed errors in the restriction requirement, the election has been treated as an election without traverse (MPEP § 818.01(a)). Claim 20 is withdrawn from further consideration pursuant to 37 CFR 1.142(b), as being drawn to a nonelected invention, there being no allowable generic or linking claim. Claims 1-17 are under examination. Drawings The drawings are objected to because the lines, shadings, numbers and letters of FIGs. 1A, 4B, 4D, 5A, 14B, 15B, 16A-B, 18A-C, and 19A-E are not sufficient to provide satisfactory reproduction characteristics. 37 CFR 1.84(l) states that “all drawings must be made by a process which will give them satisfactory reproduction characteristics. Every line, number, and letter must be durable, clean, black (except for color drawings), sufficiently dense and dark, and uniformly thick and well-defined.” In the instant case, the letters over shading in each of the gene cassette diagrams listed above are not sufficiently dark for reproduction compared to the darkness of the shadings. It is suggested that each of the shaded boxes be lightened in order to read the text in the box. Corrected drawing sheets in compliance with 37 CFR 1.121(d) are required in reply to the Office action to avoid abandonment of the application. Any amended replacement drawing sheet should include all of the figures appearing on the immediate prior version of the sheet, even if only one figure is being amended. The figure or figure number of an amended drawing should not be labeled as “amended.” If a drawing figure is to be canceled, the appropriate figure must be removed from the replacement sheet, and where necessary, the remaining figures must be renumbered and appropriate changes made to the brief description of the several views of the drawings for consistency. Additional replacement sheets may be necessary to show the renumbering of the remaining figures. Each drawing sheet submitted after the filing date of an application must be labeled in the top margin as either “Replacement Sheet” or “New Sheet” pursuant to 37 CFR 1.121(d). If the changes are not accepted by the examiner, the applicant will be notified and informed of any required corrective action in the next Office action. The objection to the drawings will not be held in abeyance. 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. Claims 15-17 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. Each of claims 15, 16 and 17 recite “A method for [therapy, diagnostics or tissue engineering], comprising the oligodendrocyte of claim 14.” A method is a series of steps. See MPEP 2106. However, there are no steps recited in the claims. Therefore, it is unclear how the claims are directed to a method and exactly how the oligodendrocytes of claim 14 are involved in the method. Claim Rejections - 35 USC § 103 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 1-17 are rejected under 35 U.S.C. 103 as being unpatentable over Du (Du et al., Mol. Cell. Neurosci . (2006), 33: 371-380) in view of Li (Li et al., Sci China Life Sci (2016), 59 : 1131–1138 , published October 25, 2016 ) and Bire (Bire and Rouleux-Bonnin. S. Renault and P. Duchateau (eds.), Site-directed Insertion of Transgenes , Problems and Solutions . Topics in Current Genetics 23 (2013) ) . Claim 9 is evidenced by Kyba (Kyba et al., Cell (2002), 109: 29-37). Regarding claims 1 -2 , 4 and 14 , Du teaches mouse embryonic stem cells (i.e., pluripotent stem cells) can be genetically modified to induce differentiation into various neural cell types including oligodendrocytes in vitro (page 371, ¶4). Regarding (a), Du teaches inserting a gene encoding rtTA (i.e., a transcriptional regulator protein) into the ROSA26 locus (i.e., a first genomic safe harbour site) (Fig 1A ; page 372, ¶2 ). Regarding (b) Du teaches inserting a gene encoding Olig2 linked to tetOP (i.e., an inducible promoter) at the HPRT locus (i.e., a second genomic safe harbour site that is different than the first site) (Fig. 1A; page 372, ¶2). Du teaches the tetOP is tetracycline inducible (i.e., the rtTA regulator protein regulates the tetOP promoter) (Fig 1A; page 372, ¶2). Du teaches inducing Olig2 expression with doxycycline (i.e., an exogenously supplied substance) promoted differentiation into oligodendrocytes (Fig 4; page 375, ¶1). Du teaches Sox10 expression was elevated by induced expression of Olig2 (page 375; ¶3). Du teaches the HPRT locus also comprised a pA sequence and an additional open reading frame. Du does not teach integrating two different transcription factors into safe harbour locus. Li teaches a method for efficient derivation of oligodendrocytes progenitor cells from human induced pluripotent stem cells (iPSCs) (i.e., a method for production of oligodendrocytes) by forced expression of two transcription factors Sox10 and Olig2 (Abstract). Li teaches transducing iPSCs with a lenti viral vector comprising the expression cassettes for Sox10 and Olig2 (page 1132, ¶3; page 1136, ¶2-4). Li teaches inducing expression of both Sox10 and Olig2 resulted in a higher percentage of oligodendrocyte progenitor cells than either Sox10 or Olig2 alone (page 1132, ¶5; Fig 2M-N). Bire teaches problems and solutions for transgene integration (Title). Bire teaches lentiviral vectors integrate preferentially around transcriptional start sites or regulatory sequences (Section 1.2.1) leading to genotoxic effects and introduc ing genomic diversity in a cell population (Section 1.3.1). Bire teaches the benefit of integration at safe harbour sites include sufficient and stable gene expression without interfering with normal cel function or gene regulation (Section 1.4.2). Bire teaches known safe harbour loci include R OSA 26 and HPRT (Section 1.4.2.2). Bire teaches the HPRT gene is located on the X chromosome in human cells and has been demonstrated has achieving tightly-controlled in vivo expression with the tetracycline system (Section 1.4.2.2). Bire teaches the ROSA26 locus in human cells is on chromosome 3 and has been demonstrated as supporting stable ubiquitous transgenes in human ES cells and derivative cell lineages (Section 1.4.2.2). Regarding claims 1-2 , 4 and 14 , it would have been obvious to one skilled in the art to have also included the SOX10 gene in Du’s HPRT-integrated tetOP-Olig2 regulated cassette. It would have amounted to the simple combination of elements by known means to yield predictable results. The skilled artisan would have predicted that the Sox10 coding sequence could be included because Du’s HPRT integrated cassette has additional transgenes and includes a pA sequence, which is a known genetic element used for co-expression of multiple genes. The skilled artisan would have been motivated to include Sox10 in addition to Olig2 because Li teaches forced expression of both genes results in a higher proportion of oligodendrocyte progenitor cells. Furthermore, the skilled artisan would have been motivated to use Du’s safe harbor approach instead of Li’s lentiviral approach because Bire teaches that lentiviral-mediated gene delivery can result in altered regulation of endogenous genes and genetic diversity within a population. Regarding claim 3, Du teaches that the rtTA protein expression is driven by the endogenous ROSA26 promoter, which is constitutively active (Fig. 1; page 372, ¶2). Regarding claims 5-6, Du teaches the rtTA protein is controlled by doxycycline, (i.e., a derivative of tetracycline) ( Fig 1B; page 372, ¶4). Regarding claim 7, Du teaches the tetOP promoter comprises a tetracycline (i.e., Tet) Respons ive Element (page 372, ¶2). Regarding claim s 8 , 10 and 12-13 , because Du’s experiments are performed in mouse ES cells, Du does not teach integration in human cells , in iPSCs, or at the hROSA26 locus or at the AAVS1 locus. As noted above for claim 1, Bire teaches the ROSA26 locus in human cells is on chromosome 3 and has been demonstrated as supporting stable ubiquitous transgenes in human ES cells and derivative cell lineages (Section 1.4.2.2). Bire also teaches the AAVS1 locus in human cells is a safe harbour locus (Section 1.4.2.2). Bire teaches AAVS1 is transcriptionally active, contains native insulators that enables resistance against transgene silencing, and no adverse effects on the cel l s due to the disruption of the endogenous gene have been detected (Section 1.4.2.2). Bire teaches one drawback to the HPRT safe harbour locus is its location on the X chromosome, which is subject to random X-inactivation (Section 1.4.2.2). Li teaches deriving oligodendrocytes from human iPSCs (Abstract). Li teaches iPSCs can be generated from a patient’s somatic cells (i.e., ex vivo) and therefore can be patient specific (page 1132, ¶2). Regarding claims 8 , 10 and 12-13 , i t would have been obvious to one skilled in the art before the effective filing date of the claimed invention to have used the obvious variant of Du’s safe-harbour integrated, tetracycline-induced Sox10 and Olig2 for oligodendrocyte differentiation specifically in human iPSCs with integrations at the hROSA26 and AAVS1 locus. It would have amounted to the simple combination of known elements by known means to yield predictable results. Regarding the use of human ex vivo iPSCs, the skilled artisan would have predicted that they could be modified similar to Du’s mouse ES cells since both cells are pluripotent and Li demonstrates delivery of transgenes to human iPSCs for oligodendrocyte differentiation. The skilled artisan would have been motivated to use iPSCs so they could be used for patient-specific cell therapies. Regarding the use of the hROSA26 and AAVS1 loci, the skilled artisan would have predicted the loci could be targeted because Bire teaches the loci have previously been used for transgene integration and have demonstrated safety profiles. Because the prior art recognizes the equivalence of HPRT and AAVS1 for the purpose of transgene integration , an express suggestion to substitute one equivalent component or process for another is not necessary to render such substitution obvious. MPEP 2144.06.II. Nevertheless, the skilled artisan would have motivated to switch from the HPRT locus to the AAVS1 locus to avoid random inactivation of integrated alleles in female-derived iPSCs. Regarding claim 9, Du teaches the ROSA26:rtTA mouse ES cell line was first developed by Kyba et al., (page 372, ¶2). Kyba teaches that the Rosa26-rtTA cell line was generated by integrating the rtTA gene into the ROSA26 locus by homologous recombination and verified by Southern blot (Fig 2; ¶ spanning pates 31-32; page 36, ¶4). Neither Du nor Kyba indicate whether one or both of the ROSA26 alleles contained the rtTA transgene. However, it would have been obvious to have screened for cells that have the rtTA transgene integrated in both alleles by Southern blot. It would have amounted to the simple duplication of elements by known means to yield predictable results. It was known in the art that homologous recombination can occur at one or both alleles and therefore predictable that at least some of the ES cells had the rtTA cassette integrated at both alleles. Even if the ROSA26-rtTA ES cells produced by Kyba only comprised the rtTA cassette at one ROSA26 allele, MPEP 2144.04 .VI.B. states that duplication of parts (i.e., the duplication of the Rosa26-rtTA locus) is prima facie obvious . Nevertheless, t he skilled artisan would have been motivated to select lines that had homozygous integration so as to increase the copy number of the rtTA cassette to increase its transcription. Regarding claim 11, as indicated above for claim 1, Bire teaches the HPRT, ROSA26 and AAVS1 sites are all safe harbour sites. Du also teaches that expression of Nkx2.2 lies upstream of Olig2 expression (page 374, ¶1). Li teaches Nkx2.2 is a marker of oligodendrocyte progenitor cells and oligodendrocytes (page 1132, ¶6). Li teaches that in another study Sox10, Olig2 and Nkx6.2 are capabl e of converting mouse fibroblasts into oligodendrocyte progenitor cells (page 1135, ¶3). It would have been obvious to one skilled in the art before the effective filing date of the claimed invention to have additionally included a third cassette comprising the additional oligodendrocyte promoter transcription factor Nkx2.2 or Nkx6.2 at a third safe harbor site. It would have amounted to the simple combination of known elements by known means to yield predictable results. The skilled artisan would have predicted that either the Nkx2.2 or Nkx6.2 could be included at a third site for producing oligodendrocytes because 1) Li teaches forced expression of three transcription factors used to producing oligodendrocyte and 2) Bire teaches a third safe harbor site useful for transgene expression. One would have been motivated to do so because Li teaches using additional transcription factors results in more efficient oligodendrocyte production. Claims 15-17 are indefinite for the reasons stated above in paragraph REF _Ref225161228 \r \h 9 . However, for the purposes of compact prosecution, each of the claims are interpreted as comprising the step of “generating the oligodendrocyte of claim 14”. Regarding claims 15 and 17, Li teaches oligodendrocytes derived from iPSCs by forced expression of Olig2 and Sox10 can be used to remyelinate axons after injury (i.e., used in therapy and tissue engineering) (page 1131, ¶1). Regarding claim 16, Li teaches further studies and demyelination models are needed to compare oligodendrocytes derived from iPSCs are transcriptionally the same as oligodendrocytes derived from embryonic stem cells (i.e., used in in vitro diagnostics) (¶ spanning pages 1135-1136). Double Patenting The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg , 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman , 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi , 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum , 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel , 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington , 418 F.2d 528, 163 USPQ 644 (CCPA 1969). A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA. A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b). The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13. The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA/25, or PTO/AIA/26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer . Claim s 1-17 are rejected on the ground of nonstatutory double patenting a s being unpatentable over claim s 1-2 and 4-23 of U.S. Patent No. 11697823 in view of Du (Du et al., Mol. Cell. Neurosci. (2006), 33: 371-380 ) and Li (Li et al., Sci China Life Sci (2016), 59 : 1131–1138 ). Patented claim 1 recites A method for controlling transcription of a genetic sequence in a cell, comprising: a) inserting into a cell a gene encoding a transcriptional regulator protein into a first genetic safe harbour site; and b) inserting into the cell an inducible cassette into a second genetic safe harbour site, wherein said inducible cassette comprises a genetic sequence operably linked to an inducible promoter, and said promoter is regulated by the transcriptional regulator protein; wherein said first and second genetic safe harbour sites are different. Patented claims 16-18 recite wherein said inserting steps are for programming of pluripotent stem cells into defined mature cells and wherein transcription of said genetic sequence results in the forward programming of the cell into a defined mature cell type. Patented claim 2 recites wherein the genetic sequence is a transgene. Patented claims 3-11 recite wherein the transcriptional regulator protein is constitutively expressed rtTA controlled by tetracycline or a derivative thereof, and the inducible promoter includes a Tet Responsive Element. Patented claim 14 recites wherein said inserting steps are performed ex vivo. Patented claim 15 recites wherein said cell is selected from a pluripotent stem cell, a somatic stem cell and a mature cell. Patented claim 19 recites wherein said cell is a human cell. Patented claims 21-23 recite A cell made by the method of claim 1 for use in therapy in vitro diagnostics or for tissue engineering. The patented claims do not recite specific transgenes for programming iPSCs for specific mature cell types. The patented claims do not recite inserting a transgene into a third genomic safe harbor site (claim 11). The teachings of Du and Li are recited above in paragraphs REF _Ref225232155 \r \h 13 , REF _Ref225232157 \r \h 15 , REF _Ref225232175 \r \h 19 - REF _Ref225232183 \r \h 22 , REF _Ref225232190 \r \h 23 , REF _Ref225232197 \r \h 25 and REF _Ref225232208 \r \h 29 and incorporated here. Briefly, Du teaches the transcriptional regulator rtTA and the oligodendrocyte (i.e., mature cell type) master regulator Olig2 linked to tetOP integrated at two different safe harbour loci. Du teaches inducing Olig2 expression with doxycycline promoted differentiation into oligodendrocytes . Li teaches forced expression of two transcription factors Sox10 and Olig2 in iPSCs resulted in a higher percentage of oligodendrocyte progenitor cells than either Sox10 or Olig2 alone . It would have been obvious to one skilled in the art before the effective filing date of the claimed invention to have modified the patented method by specifically integrating Olig2 and Sox10 at the patented safe harbor sites. It would have amounted to simple substitution of specific transcription factors known to induce oligodendrocyte differentiation from iPSCs for generic ones by known means to yield predictable results. The skilled artisan would have predicted that Olig2 and Sox10 could be used as transgenes in the patented method because Du teaches using Olig2 in a similar genetic circuit and Li teaches expressing both in iPSCs. The skilled artisan would have been motivated to do so for the purpose of producing oligodendrocytes for therapeutic purposes as taught in Du and Li. Regarding claim 11, it would have been obvious to one skilled in the art before the effective filing date of the claimed invention to have additionally modified the patented method by includ ing a third cassette comprising the additional oligodendrocyte promoter transcription factor Nkx2.2 or Nkx6.2 at a third safe harbor site. It would have amounted to the simple combination of known elements by known means to yield predictable results. The skilled artisan would have predicted that either the Nkx2.2 or Nkx6.2 could be included at a third site for producing oligodendrocytes because Li teaches forced expression of three transcription factors used to producing oligodendrocyte and the patented method recites a third and a fourth safe harbor site . One would have been motivated to do so because Li teaches using additional transcription factors results in more efficient oligodendrocyte production. Claim 14 is rejected on the ground of nonstatutory double patenting a s being unpatentable over claims 1- 27 of U.S. Patent No. 12454703 in view of Du (Du et al., Mol. Cell. Neurosci. (2006), 33: 371-380) in view of Li (Li et al., Sci China Life Sci (2016), 59 : 1131–1138 ). Patented claim 1 recites A cell, comprising: a modified genome comprising an inserted gene encoding a transcriptional regulator protein into a first genetic safe harbour site; and an inserted inducible cassette comprising a transgene operably linked to an inducible promoter into a second genetic safe harbour site, wherein said inducible promoter is regulated by said transcriptional regulator protein, and said first and second sites are different. Patented claim 13 recites wherein said transgene encodes one or more proteins for forward programming of a pluripotent stem cell into defined lineage-restricted specific stem cells, progenitor cells, or mature cells. Patented claim 20 recites A cell comprising a modified genome comprising an inserted gene encoding a transcriptional regulator protein into a first genetic safe harbour site; and an inserted inducible cassette comprising at least one transgene operably linked to an inducible promoter into a second genetic safe harbour site, wherein the inducible promoter is regulated by the transcriptional regulator protein, and the first and second sites are different, and wherein the transgene encodes at least one or more master regulators or transcription factors for forward programming. Patented claim 27 recites wherein the transgene encodes at least one or more transcription factors. The teachings of Du and Li are recited above in paragraphs REF _Ref225232155 \r \h 13 , REF _Ref225232157 \r \h 15 , REF _Ref225232175 \r \h 19 - REF _Ref225232183 \r \h 22 , REF _Ref225232190 \r \h 23 , REF _Ref225232197 \r \h 25 and REF _Ref225232208 \r \h 29 and incorporated here. Briefly, Du teaches the transcriptional regulator rtTA and the oligodendrocyte (i.e., mature cell type) master regulator transcription factor Olig2 linked to tetOP integrated at two different safe harbour loci. Du teaches inducing Olig2 expression with doxycycline promoted differentiation into oligodendrocytes. Li teaches forced expression of two transcription factors Sox10 and Olig2 in iPSCs resulted in a higher percentage of oligodendrocyte progenitor cells than either Sox10 or Olig2 alone. It would have been obvious to one skilled in the art before the effective filing date of the claimed invention to have modified the patented cell by specifically integrating Olig2 and Sox10 at the patented safe harbor sites. It would have amounted to simple substitution of specific transcription factors known to induce oligodendrocyte differentiation from iPSCs for generic ones by known means to yield predictable results. The skilled artisan would have predicted that Olig2 and Sox10 could be used as transgenes in the patented cell because Du teaches using Olig2 in a similar genetic circuit and Li teaches expressing both in iPSCs. The skilled artisan would have been motivated to do so for the purpose of producing oligodendrocytes for therapeutic purposes as taught in Du and Li. Conclusion No claims are allowable. Any inquiry concerning this communication or earlier communications from the examiner should be directed to FILLIN "Examiner name" \* MERGEFORMAT CATHERINE KONOPKA whose telephone number is FILLIN "Phone number" \* MERGEFORMAT (571)272-0330 . The examiner can normally be reached FILLIN "Work Schedule?" \* MERGEFORMAT Mon - Fri 7- 4 . Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. 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For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000. /CATHERINE KONOPKA/ Primary Examiner, Art Unit 1635