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. Drawings The drawings are objected to for the following reasons: 37 CFR 1.84 (u)(1) states “Partial views intended to form one complete view, on one or several sheets, must be identified by the same number followed by a capital letter.” In the current case, the view numbers for the partial views for Figures 7-8 that appear on several sheets are followed by "Cont." instead of a capital letter such as FIG. 1A, FIG. 1B, etc. 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. Nucleotide and/or Amino Acid Sequence Disclosures REQUIREMENTS FOR PATENT APPLICATIONS CONTAINING NUCLEOTIDE AND/OR AMINO ACID SEQUENCE DISCLOSURES Items 1) and 2) provide general guidance related to requirements for sequence disclosures. 37 CFR 1.821(c) requires that patent applications which contain disclosures of nucleotide and/or amino acid sequences that fall within the definitions of 37 CFR 1.821(a) must contain a "Sequence Listing," as a separate part of the disclosure, which presents the nucleotide and/or amino acid sequences and associated information using the symbols and format in accordance with the requirements of 37 CFR 1.821 - 1.825. This "Sequence Listing" part of the disclosure may be submitted: In accordance with 37 CFR 1.821(c)(1) via the USPTO patent electronic filing system (see Section I.1 of the Legal Framework for Patent Electronic System (https://www.uspto.gov/PatentLegalFramework), hereinafter "Legal Framework") as an ASCII text file, together with an incorporation-by-reference of the material in the ASCII text file in a separate paragraph of the specification as required by 37 CFR 1.823(b)(1) identifying: the name of the ASCII text file; ii) the date of creation; and iii) the size of the ASCII text file in bytes; In accordance with 37 CFR 1.821(c)(1) on read-only optical disc(s) as permitted by 37 CFR 1.52(e)(1)(ii), labeled according to 37 CFR 1.52(e)(5), with an incorporation-by-reference of the material in the ASCII text file according to 37 CFR 1.52(e)(8) and 37 CFR 1.823(b)(1) in a separate paragraph of the specification identifying: the name of the ASCII text file; the date of creation; and the size of the ASCII text file in bytes; In accordance with 37 CFR 1.821(c)(2) via the USPTO patent electronic filing system as a PDF file (not recommended); or In accordance with 37 CFR 1.821(c)(3) on physical sheets of paper (not recommended). When a “Sequence Listing” has been submitted as a PDF file as in 1(c) above (37 CFR 1.821(c)(2)) or on physical sheets of paper as in 1(d) above (37 CFR 1.821(c)(3)), 37 CFR 1.821(e)(1) requires a computer readable form (CRF) of the “Sequence Listing” in accordance with the requirements of 37 CFR 1.824. If the "Sequence Listing" required by 37 CFR 1.821(c) is filed via the USPTO patent electronic filing system as a PDF, then 37 CFR 1.821(e)(1)(ii) or 1.821(e)(2)(ii) requires submission of a statement that the "Sequence Listing" content of the PDF copy and the CRF copy (the ASCII text file copy) are identical. If the "Sequence Listing" required by 37 CFR 1.821(c) is filed on paper or read-only optical disc, then 37 CFR 1.821(e)(1)(ii) or 1.821(e)(2)(ii) requires submission of a statement that the "Sequence Listing" content of the paper or read-only optical disc copy and the CRF are identical. Specific deficiencies and the required response to this Office Action are as follows: Specific deficiency – Nucleotide and/or amino acid sequences appearing in FIGs. 1A, 1C , and 1E are not identified by sequence identifiers in accordance with 37 CFR 1.821(d). Sequence identifiers for nucleotide and/or amino acid sequences must appear either in the drawings or in the Brief Description of the Drawings. Required response – Applicant must provide: Replacement and annotated drawings in accordance with 37 CFR 1.121(d) inserting the required sequence identifiers; AND/OR A substitute specification in compliance with 37 CFR 1.52, 1.121(b)(3) and 1.125 inserting the required sequence identifiers into the Brief Description of the Drawings, consisting of: A copy of the previously-submitted specification, with deletions shown with strikethrough or brackets and insertions shown with underlining (marked-up version); A copy of the amended specification without markings (clean version); and A statement that the substitute specification contains no new matter. Claim Rejections - 35 USC § 101 35 U.S.C. 101 reads as follows: Whoever invents or discovers any new and useful process, machine, manufacture, or composition of matter, or any new and useful improvement thereof, may obtain a patent therefor, subject to the conditions and requirements of this title. Claim 1 and 9 are rejected under 35 U.S.C. 101 because the claimed invention is directed to a product of nature without significantly more. Step 1: Is the Claim to a Process, Machine, Manufacture, or Composition of Matter? YES. Regarding claim 1 , the claim recites a nucleic acid comprising a nucleotide sequence selected from the group consisting of a nucleotide sequence comprising at least 80% sequence identity to the claimed SEQ ID NO: 1 ( see Claim 1 ). Step 2A, Prong 1: Does the Claim Recite an Abstract Idea, Law of Nature, or Natural Phenomenon? YES. Regarding claim 1 , part (a), the appropriate counterparts to the currently claimed composition are as follows: naturally occurring [emphasis added] nucleic acid s comprising a nucleotide sequence comprising at least 80% sequence identity to the claimed SEQ ID NO s : 1 , 4, or 10 . The appropriate characteristics identified for analysis are the physical structures of the nucleic acid comprising a sequence that has at least 80% sequence identity to the claimed SEQ ID NO s : 1 , 4, or 10 . It is noted that the claimed nucleic acid is neither isolated nor in vitro. Accordingly, the claimed SEQ ID NOs: 1, 4, and 10 are directed towards a product of nature as evidenced by Nelson. Nelson is directed towards a study concerned with methods for enhancing exon skipping in a pre-mRNA of interest, comprising contacting the pre-mRNA with an effective amount of a small molecule (Abstract). Nelson teaches that Table 6 comprises suitable DMD exons that can be skipped via the use of an antisense oligonucleotide ([0056]). Nelson teaches the use of suitable exons that can have antisense oligonucleotides designed to be complementary to DMD exons selected from an exon 6 of a DMD gene that comprises a sequence that comprises 100% identity to the claimed SEQ ID NO: 1 (see SEQ ID NO: 23 in attached sequence alignment), an exon 7 of a DMD gene that comprises a sequence that has 100% identity to the claimed SEQ ID NO: 4 (see SEQ ID NO: 24 in attached sequence alignment), and an exon 8 of a DMD gene that comprises 100% identity to the claimed SEQ ID NO: 10 (see SEQ ID NO: 25 in attached sequence alignment) ([0056]-[0057]; see Table 6). Therefore, the nucleic acid comprising a nucleotide sequence comprising at least 80% sequence identity to the claimed SEQ ID NO s : 1 , 4, or 10 does not possess any markedly different characteristics when compared to naturally occurring DMD exons comprising nucleotide sequence s comprising at least 80% sequence identity to the claimed SEQ ID NO s : 1 , 4, and 10 , as taught by Nelson . Step 2A, Prong 2: Does the Claim Recite Additional Elements that Integrate the Judicial Exception into a Practical Application? NO. This judicial exception is not integrated into a practical application because there are no additional elements present in the composition. Step 2B: Does the Claim Recite Additional Elements that Amount to Significantly More than the Judicial Exception? NO. The claim does not include additional elements that are sufficient to amount to significantly more than the judicial exception because there are no additional elements present in the claim. Therefore, claim 1 is rejected under 35 USC § 101 as being drawn to a product of nature that does not possess any markedly different characteristics when compared to a naturally occurring human chromosome comprising a nucleotide sequence comprising at least 80% sequence identity to the claimed SEQ ID NO: 1 Regarding claim 9, the claim recites that the composition further comprises a carrier. The instant specification teaches that carriers may include “phosphate, citrate, or other organic acids” ([97]). Therefore, the claim is also drawn towards a product of nature because, as evidenced by Morganti ( "Citrate mediates crosstalk between mitochondria and the nucleus to promote human mesenchymal stem cell in vitro osteogenesis." Cells 9.4 (2020): 1034 ). Morganti is directed towards a study concerned with how citrate mediates crosstalk between the mitochondria and the nucleus in human stem cells (Abstract). Morganti teaches that mitochondria assemble close to the nucleus to create microdomains to facilitate the exchange of metabolites from the mitochondrial matrix to the nucleus (pg. 11) . Morganti teaches that citrate is generated in the mitochondria and exported into the nuclease and converted to αKG, which promotes histone modification, leading to transcriptional activation of genes (pg. 7, 11) . Thus, a composition comprising a carrier selected from citrate is directed towards a naturally occurring product because human cells comprise citrate in the nucleus alongside chromosomes comprising nucleic acids. 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. Claim(s) 1 is/are rejected under 35 U.S.C. 102(a)(1) as being anticipated by “AL096699” (GenBank Accession No. AL096699; published 14 March 2015). Regarding claim 1, AL096699 is directed towards a GenBank Accession No that describes a human DNA sequence on chromosome Xp21.1-21.3 (i.e., a nucleic acid) that comprises a sequence that has 100% identity to the claimed SEQ ID NO: 1 (pg. 1 and 6; see attached sequence alignment). Claim(s) 1 is/are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Nelson (PG Pub No. US 2014/0080896 A1) . Regarding claim 1, part ( a ), Nelson is directed towards a study concerned with methods for enhancing DMD exon skipping in a pre-mRNA of interest, comprising contacting the pre-mRNA with an effective amount of a small molecule (Abstract). Nelson teaches the use of DMD exons selected from an exon 6 of the DMD gene that comprises a sequence that comprises 100% identity to the claimed SEQ ID NO: 1 (see SEQ ID NO: 23 in attached sequence alignment), an exon 7 of the DMD gene that comprises a sequence that has 100% identity to the claimed SEQ ID NO: 4 (see SEQ ID NO: 24 in attached sequence alignment), and an exon 8 of the DMD gene that comprises 100% identity to the claimed SEQ ID NO: 10 (see SEQ ID NO: 25 in attached sequence alignment) ([0056]-[0057]; see Table 6). 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, 9, 11-16, and 18-20 is/are rejected under 35 U.S.C. 103 as being unpatentable over Nelson (PG Pub No. US 2014/0080896 A1) in view of Yokota ( Muscle Gene Therapy: Methods and Protocols . Totowa, NJ: Humana Press, 2010. 299-312). Regarding claim 1, part ( b ), Nelson is directed towards a study concerned with method s for enhancing exon skipping in a pre-mRNA of interest, comprising contacting the pre-mRNA with an effective amount of a small molecule (Abstract). Nelson teaches that DMD is primarily caused by out of frame multi-exon deletions in the DMD gene that ablate dystrophin protein production ([0004]). Nelson teaches that utilizing antisense oligonucleotides to promote DMD exon skipping can restore dystrophin protein expression in mice, dogs, and humans ([0004]). Nelson teaches the use of an antisense oligonucleotide that is complementary to a splicing sequence of interest ([0037]). Nelson teaches that Table 6 comprises suitable DMD exons that can be shipped via the use of an antisense oligonucleotide and that a person of ordinary skill in the art can “ readily design AO's [(i.e., antisense oligonucleotides)] specific for blocking the relevant splice sites […] without undue experimentation ” ( [0037], [0056]). Nelson teaches the use of suitable exons that can have antisense oligonucleotides designed to be complementary to DMD exons selected from an exon 6 of a DMD gene that is 170 base pairs in length and comprises a sequence that is complementary to and comprises 100% identity to the claimed SEQ ID NO: 1 (see SEQ ID NO: 23 in attached sequence alignment), an exon 7 of a DMD gene that is 119 base pairs in length and comprises a sequence that has 100% identity to the claimed SEQ ID NO: 4 (see SEQ ID NO: 24 in attached sequence alignment), and an exon 8 of a DMD gene that is 182 base pairs in length and comprises 100% identity to the claimed SEQ ID NO: 10 (see SEQ ID NO: 25 in attached sequence alignment) ([0056]-[0057]; see Table 6). Nelson teaches that the antisense oligonucleotide can be 10-50 nucleotides in length , and that in one embodiment the antisense molecules are about 17 to about 30 nucleotides in length ([0050]). Nelson teaches that the term “about” encompasses plus 10% of the indicated value ([0045]). Nelson does not specifically teach the use of a nucleotide sequence complementary to a nucleotide sequence comprising at least 80% identity to the claimed SEQ ID NOs: 1, 4, or 10 ( Claim 1 , part ( b ) ). However, one of ordinary skill in the art would have considered the teachings of Yokota as both references are common fields of endeavor pertaining to the use of antisense oligonucleotides that can skip exons in a DMD gene. Yokota is directed towards a study concerned with antisense oligonucleotide mediated multiple exon skipping in a dog model (Abstract). Yokota teaches that skipping exons 6-8 in a DMD model via the use of antisense oligonucleotides restored functional dystrophin protein production (pg. 306; see Fig. 1). Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to try to create a nucleic acid comprising a nucleotide sequence that is complementary to the nucleotide sequence comprising at least 80% identity to the sequences set forth in the claimed SEQ ID NOs: 1, 4, or, 10, as described by Nelson. A person of ordinary skill in the art would have recognized that Nelson identified a need in the art to generate antisense oligonucleotides that target and allow for the skipping of DMD exons and Yokota teaches that skipping exons 6-8 is beneficial and results in the production of functional dystrophin proteins. A person of ordinary skill in the art would have recognized that Nelson taught that there had been a finite number of possible antisense oligonucleotides that could be generated that are complementary to exons present in DMD exons 6-8 because Nelson teaches that exon 6 of the DMD gene only comprises 170 base pairs, exon 7 only comprises 119 base pairs, and exon 8 only comprises 181 base pairs alongside an explicit disclosure that in one embodiment the antisense molecule is 10-50 nucleotides in length or about 17 to about 30 nucleotides in length, wherein the term “about” encompasses plus 10% of the indicated value. Therefore, the amount of experimentation required to arrive at a nucleotide sequence that is complementary to the nucleotide sequence comprising at least 80% identity to the claimed SEQ ID NOs: 1, 4, or 10 is not large because Nelson provides evidence that all three exons are less than 200 base pairs in length and that antisense oligonucleotides targeting the exons can be designed such that they are 10-50 base pairs, or about 17 base pairs to about 30 base pairs, in length and tested to ensure that the antisense oligonucleotides induce skipping of a targeted exon without undue experimentation. A person of ordinary skill in the art would have recognized that the known potential solutions could have been pursued because Nelson explicitly states that a person of ordinary skill in the art can readily design antisense oligonucleotides specific for blocking the relevant splice sites present in the exons of Table 6. Regarding claim 9, Nelson teaches that a dosage comprising the therapeutic agent (i.e., the antisense oligonucleotide ([0065])) may comprise a pharmaceutically acceptable carrier ([0068]). Regarding claim 11, Nelson teaches that the disclosed antisense oligonucleotides can be administered to a subject to treat muscular dystrophy ([0057]). Regarding claims 12-13, Nelson teaches that the antisense oligonucleotides may be administered to a subject via subcutaneous injection ([0063]). Regarding claim 14, Nelson teaches that the muscular dystrophy may be Duchenne Muscular Dystrophy (i.e., DMD) ([0055]). Regarding claim 15, Nelson teaches that DMD is caused by multi-exon deletions in the DMD gene that ablate dystrophin protein production ([0004]). Nelson teaches that administering effective doses of the antisense oligonucleotides results in an inducing at least a detectable amount of dystrophin expression with targeted removal of a given exon (i.e., the introduction of the antisense oligonucleotide results in an increased level of functional dystrophin protein when compared to a level of functional dystrophin protein produced prior to the introduction) ([0046]). Regarding claim 16, Nelson teaches that the level of dystrophin protein production following administration of the antisense oligonucleotide can be measured via the use of Western blot ([0009]; see FIG. 3). Regarding claim 18, Nelson teaches that dantrolene can be utilized as a modulator of antisense-mediated exon skipping in DMD ([0007]); Nelson teaches that dantrolene, when administered to a synergistically with an antisense oligonucleotide, resulted in improved muscle strength in mice ([0027]). Regarding claim 19, Nelson does not teach that a 6 minute walk test was utilized to measure improved muscle function in a subject (Claim 19). However, Nelson further teaches that previous studies had utilized a 6 minute walk test to subjects who received antisense oligonucleotides directed against DMD exon 51 ([0005]). Nelson teaches that the subjects who received the antisense oligonucleotides showed a modest improvement in the test ([0005]). Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to utilize a 6 minute walk test as a measurement of muscular dystrophy progression, as described by Nelson. A person of ordinary skill in the art would have been motivated to do so in order to utilize a known method of determining if the antisense oligonucleotides successfully skipped exons in a subject such that their muscular dystrophy progression was able to be measured and ultimately reversed such that improvements in the test were demonstrated. A person of ordinary skill in the art would have had a reasonable expectation of success because Nelson in view of Yokota teach that it was known in the art that utilizing a 6 minute walk test to confirm the successful exon skipping, mediated by antisense oligonucleotides, in subjects of interest was a known method of measuring muscular dystrophy progression. Regarding claim 20, Nelson teaches that a second combination therapeutic agent may be administered to a subject and present within a kit comprising the antisense oligonucleotide ([0086]). Claim(s) 2-3 is/are rejected under 35 U.S.C. 103 as being unpatentable over Nelson (PG Pub No. US 2014/0080896 A1) in view of Yokota ( Muscle Gene Therapy: Methods and Protocols . Totowa, NJ: Humana Press, 2010. 299-312) as applied to claim s 1, 9, 11-16, and 18-20 above, and further in view of Sazani (US Patent No. 9,234,198 B1). Regarding claims 2-3, Nelson in view of Yokota renders obvious claims 1, 9, 11-16, and 18-20 as described above. Nelson in view of Yokota does not teach or suggest that the nucleic acid comprises a combination of a nucleotide sequence that targets the human DMD gene at exons 6 and 7 (Claim 2) or a combination of exons 6-8 (Claim 3). However, one of ordinary skill in the art would have considered the teachings of Sazani as both references are common fields of endeavor pertaining to the use of antisense oligonucleotides that can be utilized to skip DMD exons. Sazani is directed towards an invention concerned with antisense molecules capable of binding to a selected target site in the human dystrophin gene to induce exon skipping (Abstract). Sazani teaches that it is possible to combine two or more antisense oligonucleotides together to induce multiple exon skipping and that the combination of antisense oligonucleotides improves multiple exon skipping (Col. 3, lines 40-49). Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to modify the antisense oligonucleotides of Nelson in view of Yokota such that the nucleic acid comprised nucleotide sequences that targeted exons 6-8 of a human DMD gene, as described by Sazani . A person of ordinary skill in the art would have been motivated to do so in order to improve multiple exon skipping of exons 6-8 in a human DMD gene. A person of ordinary skill in the art would have had a reasonable expectation of success because both Sazani and Nelson in view of Yokota teach the use of antisense oligonucleotides that can target human DMD genes and induce exon skipping. Claim(s) 4 is/are rejected under 35 U.S.C. 103 as being unpatentable over Nelson (PG Pub No. US 2014/0080896 A1) in view of Yokota ( Muscle Gene Therapy: Methods and Protocols . Totowa, NJ: Humana Press, 2010. 299-312) as applied to claims 1, 9, 11-16, and 18-20 above , and further in view of Flanigan (PG Pub No. US 2017/0218366 A1). Regarding claims 4 , Nelson in view of Yokota renders obvious claims 1, 9, 11-16, and 18-20 as described above. Nelson further teaches that the antisense oligonucleotides can be administered via the use of an AAV expression vector ([0047]). Nelson in view of Yokota does not teach or suggest that the nucleic acid comprises a nucleotide sequence that is at least 70% identical to the claimed SEQ ID NO: 26 (Claim 4). However, one of ordinary skill in the art would have considered the teachings of Flanigan as both references are common fields of endeavor pertaining to the use of AAV vectors to deliver antisense molecules to a cell of interest. Flanigan is directed towards an invention concerned with methods for enhancing exon skipping in a pre-mRNA of interest , including methods that can treat DMD ( Abstract ). Flanigan teaches the use of an AAV vector that comprises a genome insert that comprises 83.6% identity to the claimed SEQ ID NO: 26 ( [0037]- [0038]; see SEQ ID NO: 26 in attached sequence alignment). Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to substitute the AAV delivery vector rendered obvious by Nelson in view of Yokota for an AAV vector comprising a nucleotide sequence that has at least 70% identity to the claimed SEQ ID NO: 26, as described by Flanigan . A person of ordinary skill in the art would have had a reasonable expectation of success because both Flanigan and Nelson in view of Yokota teach the use of AAV vectors that can deliver antisense nucleic acid molecules. Claim(s) 5-8 and 10 is/are rejected under 35 U.S.C. 103 as being unpatentable over Nelson (PG Pub No. US 2014/0080896 A1) in view of Yokota ( Muscle Gene Therapy: Methods and Protocols . Totowa, NJ: Humana Press, 2010. 299-312) as applied to claims 1, 9, 11-16, and 18-20 above , and further in view of Kaspar (PG Pub No. WO 2019/236949 A1). Regarding claims 5-8 and 10 , Nelson in view of Yokota renders obvious claims 1, 9, 11-16, and 18-20 as described above. Nelson further teaches that the antisense oligonucleotides can be administered via the use of an AAV expression vector ([0047]). Nelson in view of Yokota does not teach or suggest th e use of an rAAV comprising the antisense oligonucleotide (Claims 5 and 10) selected from rAAV9 (Claims 6-7) that is self-complementary (Claim 8). However, one of ordinary skill in the art would have considered the teachings of Kaspar as both references are common fields of endeavor pertaining to the use of vectors encoding antisense nucleic acids. Kaspar is directed towards an invention concerned with transgene-expressing viral vector drug product s (Abstract). Kaspar teaches the use of a vector comprising an rAAV9 genome to deliver nucleic acids of interest to a cell ([00126]). Kaspar teaches the use of an rAAV9 genome that can encode an antisense molecule ([00228]). Kaspar teaches that rAAV genome can be self-complementary ([00278]). Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to substitute the delivery vector rendered obvious by Nelson in view of Yokota for an rAAV9 vector or a vector that is self-complementary, as described by Kaspar . A person of ordinary skill in the art would have had a reasonable expectation of success because both Kaspar and Nelson in view of Yokota teach the use of vectors that can encode antisense oligonucleotides. Claim(s) 17 is/are rejected under 35 U.S.C. 103 as being unpatentable over Nelson (PG Pub No. US 2014/0080896 A1) in view of Yokota ( Muscle Gene Therapy: Methods and Protocols . Totowa, NJ: Humana Press, 2010. 299-312) as applied to claims 1, 9, 11-16, and 18-20 above , as evidenced Be t orini ( Official Journal of the American Association of Electrodiagnostic Medicine 14.6 (1991): 503-507). Regarding claims 7 , Nelson in view of Yokota renders obvious claims 1, 9, 11-16, and 18-20 as described above. Nelson further teaches that dantrolene can be synergistically administered alongside the antisense oligonucleotide ([0007]) . Nelson in view of Yokota does not teach or suggest that the level of serum creatine kinase is decreased after administration of a composition comprising the nucleic acid molecule (Claim 17). However, one of ordinary skill in the art would have considered the teachings of Betorini as both references are common fields of endeavor pertaining to the study of dantrolene and its effects when administered to subjects who have DMD. Betorini is directed towards a study concerned with the effect of dantrolene in DMD (Abstract). Betorini teaches that dantrolene reduces serum creatine kinase in subjects who have DMD (Abstract). Therefore, as evidenced by Betorini , the composition comprising the nucleic acid molecule and dantrolene rendered obvious by Nelson in view of Yokota would have resulted in the reduction of serum creatine kinase in a subject who was administered the composition, as evidenced by Betorini . A person of ordinary skill in the art would have recognized that Betorini teaches that dantrolene decreases the amount of serum creatine kinase in subjects who had DMD while Nelson in view of Yokota renders obvious the administration of dantrolene to subjects who have DMD. Claim(s) 21 is/are rejected under 35 U.S.C. 103 as being unpatentable over Nelson (PG Pub No. US 2014/0080896 A1) in view of Yokota ( Muscle Gene Therapy: Methods and Protocols . Totowa, NJ: Humana Press, 2010. 299-312) as applied to claims 1, 9, 11-16, and 18-20 above , further in view of Manzur ( Cochrane database of systematic reviews 1 (2008) ). Regarding claim 21 , Nelson in view of Yokota renders obvious claims 1, 9, 11-16, and 18-20 as described above. Nelson in view of Yokota does not teach or suggest that the method further comprises administering a glucocorticoid (Claim 21). However, one of ordinary skill in the art would have considered the teachings of Manzur as both references are common fields of endeavor pertaining to the treatment of DMD. Manzur is directed towards a study concerned with the use of glucocorticoid corticosteroids for the treatment of DMD (pf. 1). Manzur teaches that administering glucocorticoid corticosteroids improved muscle strength and function over six months (pg. 2) . Manzur teaches that i mprovements were seen in time taken to rise from the floor (Gowers' time), nine meters walking time, four‐stair climbing time, ability to lift weights, leg function grade and forced vital capacity (pg. 2). Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to modify the method rendered obvious by Nelson in view of Yokota such that it further comprise d administering a glucocorticoid , as described by Manzur . A person of ordinary skill in the art would have been motivated to do so in order to improve muscle strength in a subject who had DMD. A person of ordinary skill in the art would have had a reasonable expectation of success because Nelson in view of Yokota teaches that the antisense oligonucleotide can be utilized in a method of treating DMD while Manzur teaches that administering a glucocorticoid to a subject who had DMD was a known beneficial compound that aided in the treatment of the disease. Conclusion Any inquiry concerning this communication or earlier communications from the examiner should be directed to FILLIN "Examiner name" \* MERGEFORMAT KYLE T REGA whose telephone number is FILLIN "Phone number" \* MERGEFORMAT (571)272-2073 . The examiner can normally be reached FILLIN "Work Schedule?" \* MERGEFORMAT M-R 8:30-4:30, every other F 8:30-4:30 (EDT/EST) . Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice. If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, FILLIN "SPE Name?" \* MERGEFORMAT Neil Hammell can be reached at FILLIN "SPE Phone?" \* MERGEFORMAT 571-270-5919 . The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300. Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. 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. /KYLE T REGA/ Examiner, Art Unit 1636 /NEIL P HAMMELL/ Supervisory Patent Examiner, Art Unit 1636