DETAILED ACTION Claims 1-6, 8, 9, 11, 13, 14, 16-19, 21, 23, 26, 46, 54, 60, 64, 66, 123, and 124 are currently pending. Claims 7, 10, 12, 15, 20, 22, 24-25, 27-45, 47-53, 55-59, 61-63, 65, 67-122 and 125-152 are cancelled. 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. Election/Restrictions Applicant’s election without traverse of Group I (claims 1-6, 8, 9, 11, 13, 14, 16-19, 21, 23, 26, 46, 54, 60, 64, and 66) in the reply filed on 10/6/2025 is acknowledged. Applicant’s election with traverse of Group I cell-type of epicardial progenitor cells (claims 13-14) is further acknowledged. Applicant notes the present methods produce a heterogenous population of cardiac progenitor cells from more than one developmental lineage including epicardial progenitor cells, endothelial fibroblast progenitor cells, and second heart field progenitor cells which should be considered for the search and examination. It is initially reiterated that the requirement to elect a single species is contingent on the non-allowability of the generic claim(s). As is proper in election of species practice, should a generic claim be found allowable the search will be extended to include additional species, see MPEP § 809.02. At this time, however, no generic claim has been found allowable, and the recited species are considered to be patentably distinct from one another for the reasons set forth in the previous Office action at pages 6-7. Specifically, each of the species of cell types: (a) second heart field progenitor cells (express GATA4/HAND2) ; (b) endothelial fibroblast progenitor cells (express TEK) ; (c) epicardial progenitor cells (express WT1) ; and (d) cardiac fibroblasts (express COL1A1) , have distinct phenotypes from one another , and, thus, differently searched . In light of such, performance of a comprehensive search for one of the types of progenitor cells would not necessarily result in a complete or comprehensive search for any one or more of the other types of progenitor cells. Execution of a search encompassing all of Applicant's presently claimed species would constitute an undue burden on the Examiner, since the types of progenitor cells are sufficiently disparate in nature such that one of the types of progenitor cells would not necessarily anticipate or render obvious the other types of progenitor cells. Furthermore, consideration of the findings of such a search in accordance with the requirements of the law under 35 USC §§ 101, 102, 103 and 112 would be unduly onerous. Thus, the election of species requirement as indicated in the previous Office Action is maintained as proper and hereby made FINAL. Claims 6, 8-9, 11, 17-19, 21, 54, 60, 64-66 and 123-124 are withdrawn. Priority Acknowledgement is made of the instant application being a national stage entry under 35 USC 371 of international application PCT/ US2023 /0 75750 , filed 10/2/2023 , which claims the benefit of provisional application No. 6 3 / 412 , 212 , filed 9/30/2022. Information Disclosure Statement The information disclosure statement (IDS) submitted on 9/16/2024 is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner. The listing of references in the specification (pages 59-61) is not a proper information disclosure statement. 37 CFR 1.98(b) requires a list of all patents, publications, or other information submitted for consideration by the Office, and MPEP § 609.04(a) states, "the list may not be incorporated into the specification but must be submitted in a separate paper." Therefore, unless the references have been cited by the examiner on form PTO-892, they have not been considered. Drawings The drawings are objected to because the text in FIG. 4H is illegible. 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 Claim s 1-5, 13-14, 16, 23, 26 and 46 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 . Claim 1 as currently written encompass es conducting each of the three steps (a-c) for any culture time period (e.g., 1 second or 1 year) and using any concentration (e.g., 0.00000 pg /ml) of the various factors for each of the differentiation steps . Dependent claims 2-5, 13-14, 16, 23, 26 and 46 depend directly from claim 1, or incorporate the method of claim 1. FIGS 1, 2A and 3A exemplify in vitro methods for producing fibroblast progenitor cells from human pluripotent stem cells. These illustrations show directed differentiation employing specific factors for specific time periods and using specific concentrations of the various differentiation factors. FIG 2A specifically illustrates the ABC method to produce WT+ epicardial progenitor cells and the specification at [0052] discloses the ABC method comprises: Using Activin A (9 ng/ml) , BMP4 (5 ng/ml) , and CHIR (7 µM) on Day 1 and Activin and BMP only were added on Day 2 of differentiation. The specification further provides Example 1 ([00216]-[0021 9 ]) differentiation method to produce highly pure populations of iPSC-derived quiescent cardiac fibroblasts, such as from a population of (WT1+) epicardial cells wherein a starting population of iPSCs were formed into aggregates in a low concentration of GSK3 inhibitor in E8 medium comprising ROCK inhibitor (Table 1). On Day 1, iPSCs were treated with a high level GSK3 (CHIR99021) inhibitor for one day in the presence of Activin A and BMP4 growth factors in RPMI/B27 minus insulin containing medium for cardiac mesoderm induction. On day two no GSK3 inhibitor was used and Activin A and BMP4 growth factors were refreshed. This is termed ABC mesoderm inductio n, and by Day 3 of the ABC method , a population of NCAM+/ CXCR4 low positive- mesoderm progenitor cells were produced (FIG. 2A). It was observed that Activin A and BMP4 in addition to CHIR during mesoderm induction resulted in a decreased percentage of CXCR4+ progenitors compared to CHIR alone. For ABC conditions, 9 ng/mL Activin A, 5 ng/mL BMP4, and 7 uM CHIR99021 (Table 2) were added on Day 1 and Activin A and BMP4 only (Table 3) were added on Day 2 of differentiation. Cardiac mesoderm cells were then dissociated and contacted with a low concentration of Wnt inhibitor, XAV939, (Table 4) for two days to be specified into a WT1 epicardial lineage (FIG. 3A). Upon review of the specification, the specification shows that Applicants have not provided sufficient description of the invention to support they were in possession of : An in vitro method for producing human pluripotent stem cell (PSC)-derived cardiac fibroblast progenitor cells comprising: (a) culturing PSC aggregates for any time period in media comprising a ny amount of Wnt agonist, any amount of Activin agonist, and any amount of BMP4 for mesoderm induction; (b) further culturing the PSC aggregates for any time period in media comprising an y amount of Activin agonist and any amount of BMP4 and essentially free of a Wnt agonist to produce a population of mesoderm progenitor cells; and (c) culturing the mesoderm progenitor cells for any time period in media comprising a ny amount of Wnt inhibitor to produce a population of cardiac fibroblast progenitor cells, wherein the cardiac fibroblast progenitor cells comprise epicardial progenitor cells, endothelial fibroblast progenitor cells, and second heart field progenitors. Possession of an invention may be shown in a variety of ways including description of an actual reduction to practice, or by showing that the invention was "ready for patenting" such as by the disclosure of drawings or structural chemical formulas that show that the invention was complete, or by describing distinguishing identifying characteristics sufficient to show that the applicant was in possession of the claimed invention. See, e.g., Pfaff v. Wells Elecs., Inc. , 525 U.S. 55, 68, 119 S.Ct . 304, 312, 48 USPQ2d 1641, 1647 (1998). In the instant case the only references in the specification to an in vitro method for producing human pluripotent stem cell (PSC)-derived cardiac fibroblast progenitor cells are directed to using specific culturing time periods and specific concentrations of the various differentiation factors (FIG. 1, 2A, 3A; Example 1). Thus, a review of the specification shows that Applicants have not provided sufficient description of the invention as currently claimed. Accordingly, the claims are considered to lack sufficient written description and are properly rejected under 35 USC 112, first paragraph. The following is a quotation of 35 U.S.C. 112(d): (d) REFERENCE IN DEPENDENT FORMS.—Subject to subsection (e), a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers. The following is a quotation of pre-AIA 35 U.S.C. 112, fourth paragraph: Subject to the following paragraph [i.e., the fifth paragraph of pre-AIA 35 U.S.C. 112], a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers. Claim 26 is rejected under 35 U.S.C. 112(d) or pre-AIA 35 U.S.C. 112, 4th paragraph, as being of improper dependent form for failing to further limit the subject matter of the claim upon which it depends, or for failing to include all the limitations of the claim upon which it depends. Claim 26 recites: “ The method of claim 24, wherein the iPSCs are derived from a subject with dilated cardiomyopathy and comprise an LMNA-L35P mutation .” Claim 26 depends directly from a cancelled claim, claim 24. Applicant may cancel the claim(s), amend the claim(s) to place the claim(s) in proper dependent form, rewrite the claim(s) in independent form, or present a sufficient showing that the dependent claim(s) complies with the statutory requirements. 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. The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows: 1. Determining the scope and contents of the prior art. 2. Ascertaining the differences between the prior art and the claims at issue. 3. Resolving the level of ordinary skill in the pertinent art. 4. Considering objective evidence present in the application indicating obviousness or nonobviousness . 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 -5 ,13-14, 16, 23 and 46 are rejected under 35 U.S.C. 103 as being unpatentable over Keller et al., (US 2016/215263; IDS 9/16/2024) (“Keller”) , in view of Mendjan et al., (WO 2021/186044; IDS 9/16/2024) (“ Mendjan ”) and Guadix et al . , ( Stem Cell Reports, Vol. 9, 1754-1764, 2017 and Supplemental Information, 10 pages; see PTO-892) (“ Guadix ”) , as evidenced by van den Heuvel- Eibrink MM, editor. Wilms Tumor [Internet]. Chapter 13 WT1 in Cardiac Development and Disease , Brisbane (AU): Codon Publications; 2016 Mar , retrieved from the Internet (see PTO-892) (“ Duim ”). Keller teaches a method for obtaining cardiomyocyte lineage or an epicardial lineage cell population from human pluripotent stem cells via directed differentiation induced by exposure to defined chemicals at certain stages (Abstract) . Keller is directed to developing culture systems that more accurately represent the human heart for therapeutic applications ([0008]). Regarding claim 1, Keller’s F IG 1 ([0012]) depicts the scheme of the in vitro protocol used to differentiate hESCs (i.e., pluripotent stem cells) towards the cardiomyocyte lineage highlighting the three main stages of development: 1) mesoderm induction using BMP4, Activin A and bFGF , 2) cardiovascular specification using Wnt inhibitor DKK1, and 3) maturation ( maintained in VEGF for 9 days and then analyzed for the presence of cTnT + cardiomyocytes by flow cytometry ) . Keller acknowledges that BMP4 and Wnt components (e.g., CHIR99021 Wnt agonist) are epicardial lineage - promoting components and promote WT1+ epicardial progenitor cells ([0028] and [0044]) (claims 1 and 5) . Keller further teaches the effective concentrations/combinations of BMP4 and the Wnt component can be determined by monitoring and optimizing for WT1 or TBX18 expression ( [0044] ) . Although Keller differs from claim 1, step ( a ) in that Keller’s FIG 1 does not show the presence of a Wnt agonist at mesoderm induction (in combination with Activin and BMP4) , it is noted that Keller’s FIG 10 (A-B) ([0012]) shows the presence of the Wnt agonist CHIR (CHIR 99021) , during mesoderm induction to generate WT1+ epicardial progenitor cells and Mendjan teaches in vitro methods for generating cardiac tissue models (e.g. epicardial cells) from pluripotent stem cells using directed differentiation (Abstract; page 2 at last two paragraphs to page 3, first paragraph) wherein Wnt activation promotes mesoderm differentiation, and Mendjan teaches this works especially well when the Wnt activation is combined with BMP4, bFGF and Activin A (page 14, first paragraph) . It is further noted that Guadix is directed to in vitro methods for differentiation of human pluripotent stem cells (embryonic and induced) into functional epicardial progenitor cells (i.e., cardiac fibroblast progenitor cells ) since these cells have potential for therapeutic use for cardiac regeneration (Summary). Figure 1B of Guadix illustrates methods of proepicardial differentiation of hESCs (i.e., human pluripotent stem cells ) wherein mesoderm induction employs Activin A (ACT-A), BMP4 and the Wnt agonist CHIR-99021. Figure 1B is copied below : Figure S1 of Guadix likewise discloses an in vitro method for producing human pluripotent stem cell-derived epicardial progenitor cells (Stem Cell Reports vol 9, Supplemental Information) wherein mesoderm induction employs Activin A (ACT-A), BMP4 and the Wnt agonist CHIR-99021 . Guadix , (see Supplemental Information , Monolayer differentiation of hPSC to epicardial-like cells ) , teaches differentiation to epicardial-like cells by seeding 20 × 10 3 /cm 2 of both hESC (i.e., human pluripotent stem cells) and wild-type hiPSC (i.e. human induced pluripotent stem cells) on plates coated with 75 µg/mL of Matrigel (growth factor reduced) the day before differentiation (day -1). At day 0, cardiac mesoderm was induced (i.e., mesoderm induction ) by changing E8 to BPEL medium supplemented with a mixture of cytokines comprising BMP4, ACTIVIN A (activin agonist) and GSK3 inhibitor CHIR99021 (Wnt agonist), as recited in claim 1, step a. After 3 days, the cytokines were removed and the culture was supplemented with the WNT inhibitor XAV939 for 3 days together with RA (1 μM ) and BMP4 (30 ng/ml). Therefore, taking into hand the teachings of Keller, Mendjan and Guadix , it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to include a Wnt agonist , in combination with BMP4 and Activin A, for mesoderm induction. The person of ordinary skill in the art would have been motivated to include a Wnt agonist that is known to promote mesoderm induction , as taught by each of Keller, Mendjan and Guadix , for the predictable result of successfully promoting WT1+ epicardial progenitor cells , thus meeting the limitation of claim 1. The skilled artisan would have had a reasonable expectation of success in combining the teachings of Keller with Mendjan and Guadix because each of these teachings are directed at methods of directed differentiation of human pluripotent stem cells to produce various lineages of therapeutic cardiac cells, including epicardial progenitor cells . As to claim 1, step c, Keller (Figure 1) teaches subjecting the mesoderm progenitor cells to culturing in the presence of a Wnt inhibitor, i.e., DKK1, thus meeting the limitation of claim 1. As to claim 1, step b and claim 2 , it is initially noted regarding the limitation: “…essentially free of a Wnt agonist…” the specification at [0072] discloses the phrase “essentially free” means that none of the specified component has been purposefully formulated into a composition and/or is present only as a contaminant or in trace amounts. The total amount of the specified component resulting from any unintended contamination of a composition is therefore well below 0.05%, preferably below 0.01%. Thus, the specification has provided clarity regarding the guidelines to delineate between essential ingredients, purposely added to the culture media, and unavoidable contaminants or trace amounts, in that a Wnt agonist that is present below 0.05% meets the limitation of claim 1. I t is noted the combined prior art does not specifically teach culturing in the presence of Activin agonist (Activin A) and BMP4, and “ essentially free of a Wnt agonist ” (claim 1) or “free of a Wnt agonist” (claim 2) . However, it is noted that Keller acknowledges that Wnt agonist components (e.g., CHIR99021) are epicardial lineage promoting components and promote WT1+ epicardial progenitor cells ([0028] and [0044]) and the combinations of these factors can be optimized by monitoring the expression of mesoderm markers WT1 and TBX18 , and Mendjan further teaches that differentiation of the mesoderm cells into more mature cardiac cells can be conducted in the absence of the Wnt activator (agonist) for a few days (i.e., essentially free of a Wnt agonist ) , and thereafter subjected to a Wnt antagonist (inhibitor) to promote the cells leaving the mesoderm stage (page 15, last paragraph to page 16, first paragraph) . Thus, it is well within the purview of the skilled artisan to optimize the presence or absence of the differentiation factors based on WT1 or TBX18 expression levels, and when the desired threshold is met, it would be obvious to one of ordinary skill in the art to remove/decrease the amount of Wnt agonist in order to optimize the differentiation lineage and promotion of differentiation to the desired epicardial progenitor phenotype . Regarding claims 3-4 and the limitations directed to mesoderm progenitor cells are positive for NCAM and have low expression of CXCR4 (claim 3) and wherein less than 10% of the mesoderm progenitor cells are positive for CXCR4 (claim 4), it is noted the specification at [00218] discloses that by day 3 of culturing using Activin A and BMP4, in combination with CHIR (Wnt agonist), a mesoderm population that has NCAM+/ CXCR4 low phenotype has developed , thus mesoderm differentiation results in the claimed phenotype. It is noted the combined prior art does note further comment on the expression of NCAM or CXCR4. However, the combined prior art teaches mesoderm differentiation in the presence of the same Activin A, BMP4, CHIR-99021 (Wnt agonist) and identifies the cells being WT1+ cells. It is further noted that Duim et al acknowledges that NCAM is coexpressed in WT1+ epicardial cells ( Clinical perspective , third paragraph). Therefore, although the combined prior art does not state the mesoderm progenitor cells are positive for NCAM and have low expression of CXCR4 (claim 3) and wherein less than 10% of the mesoderm progenitor cells are positive for CXCR4 (claim 4), the fact that the prior art carries out the same method steps as in the instant application means that any and all results of the method of the prior art, whether recognized at the time of publication or not, were inherently achieved by the prior art. Regarding claims 13 -14 and 46 , it is noted that Keller teaches the epicardial progenitor cells are positive for WT1, thus meeting the limitation of claim 14. As to claim 13 and the limitation directed to the percentage of cells that are epicardial progenitor cells, i.e., 5-40%, it is noted Keller’s intention of directed differentiation is to specify a WT1+ cardiovascular progenitor cell population ( Abstract ). Keller at FIG. 4 ([0015]) shows expression of myocardial and epicardial markers after BMP treatment at days 6, 8, 10, 12, and 15 of culture in populations generated from no treatment (control), BMP4 treated (mesoderm induction) or Noggin (400 ng/ml) treated cells, wherein D8, D10 and D12 expression reads on “about 5-40%” as recited in claim 13 and “at least 30%” as recited in claim 46 . Additionally, FIG. 8D shows the WT1 and TBX18 expression levels in the PDGFRα+ mesoderm cells wherein about 40% of the cell population has positive expression of WT1. Regarding claim 16 and the limitation that step (c) is further defined as producing a mixed population of cardiac fibroblast progenitor cells and cTNT + cardiomyocytes, it is noted Keller, at FIG. 8A-D, shows analyzing the cell cultures for expression of WT1 and cTNT (i.e., cTNT + cardiomyocytes), wherein the data shows development of cTNT expression over the 15 day culture, and positive expression of WT1+, which reads on producing a mixed population of cardiac fibroblast progenitors and cTNT + cardiomyocytes, thus meeting the limitation of claim 16. Regarding claim 23 , Keller teaches the pluripotent stem cells are hESCs (human embryonic stem cells) or induced pluripotent stem cells ([0012], [0021]) and [0124]), thus meeting the limitation of claim 23. Claim(s) 26 is rejected under 35 U.S.C. 103 as being unpatentable over Keller , in view of Mendjan and Guadix , as evidenced by Duim , as applied to claims 1-5 ,13-14, 16, 23 and 46 above, and further in view of Steele- Stellard et al., ( Frontiers in Physiology , October 2018, vol. 9, Article 1332, 19 pages) (“Steele-Stallard”) . The teaching of Keller , in view of Mendjan and Guadix , as evidenced by Duim is set forth above. Claim 26 recites the limitation “ wherein the iPSCs are derived from a subject with dilated cardiomyopathy and comprise an LMNA-L35P mutation . ” The cited prior art does not further comment on using iPSCs that are derived from a subject with dilated cardiomyopathy and comprise an LMNA-L35P mutation . However, Steele-Stallard is directed to us ing induced pluripotent stem cells (iPSCs) from patients with skeletal muscle laminopathies such as LMNA-related congenital muscular dystrophy and limb-girdle muscular dystrophy 1B, to model disease phenotypes in vitro since iPSCs can be derived from readily accessible cell types, have unlimited proliferation potential and can be differentiated into cell types that would otherwise be difficult and invasive to obtain (Abstract) . Mutations in LMNA cause at least 16 rare disorders, collectively known as laminopathies and include dilated cardiomyopathy (Introduction, page 2, left col, second paragraph). Steele-St a llard further teaches that induced pluripotent stem cells (iPSCs) offer a new approach to disease modeling and drug screening and the iPSCs can be made from patient primary cells obtained from minimally invasive sources, such as skin fibroblasts, blood or urine cells, which can then be reprogrammed to pluripotency and directed to differentiate into any cell type, enabling the study of disease-/patient-specific cells that would otherwise be difficult to obtain (Introduction, page 2, right col, second paragraph) . Steele-St a llard teaching employing the LMNA-35P iPSCs for differentiation studies to generate an expandable population of mesodermal cells (page 3, right col, first paragraph; Discussion, page 11, right col, last paragraph) and notes that using LMNA-mutant iPSCs to model muscle laminopathies could provide the foundations for next-generation therapy screening platforms to tackle this group of severe and incurable disorders (page 13, right col, first full paragraph) . Therefore, given the intention of Keller is to develop culture systems representing the human heart for therapeutic applications ([0008]), it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to obtain the pluripotent stem cells from subjects with dilated cardiomyopathy and comprising an LMNA-L35P mutation since Steele-Stallard teaches the cells are readily available , have unlimited proliferation potential and can be differentiated into cell types that would otherwise be difficult and invasive to obtain . The person of ordinary skill in the art would have been motivated to modify the prior art method to include obtain ing the pluripotent stem cells from subjects with dilated cardiomyopathy and comprising an LMNA-L35P mutation , as taught by Steele-Stallard , for the predictable result of successfully permitting development of cell-based disease models for future therapeutic use, thus meeting the limitation of claim 26 . The skilled artisan would have had a reasonable expectation of success in combining the prior art teachings with Steele-Stallard because each of these teachings are directed at using induced pluripotent stem cells for disease modeling and therapeutic research. Conclusion No claim is allowed. No claim is free of prior art. Examiner Contact Information Any inquiry concerning this communication or earlier communications from the examiner should be directed to FILLIN "Examiner name" \* MERGEFORMAT E. 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To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. 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. FILLIN "Examiner Stamp" \* MERGEFORMAT E. YVONNE PYLA Primary Examiner Art Unit 1633 /EVELYN Y PYLA/ Primary Examiner, Art Unit 1633