CTFR 17/779,372 CTFR 100719 DETAILED ACTION Notice of Pre-AIA or AIA Status 07-03-aia AIA 15-10-aia The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA. Applicant’s submission filed on March 2, 2026 has been entered and considered. Rejections and/or objections not reiterated from the previous action mailed December 1, 2025 are hereby withdrawn. The following rejections and/or objections are either newly applied or are reiterated and are the only rejections and/or objections presently applied to the instant application. The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action. Election/Restrictions Applicant’s election of Group 1, claims 1-18 and 21 drawn to an artificial transcription factor system in the reply filed on September 2, 2025 is acknowledged. Because applicant did not distinctly and specifically point out the supposed errors in the restriction requirement, the election was treated as an election without traverse (MPEP § 818.01(a)). Applicant has elected the species of p65 as the gene modulating domain and IL2RA as the target gene. In view of the prior art, the HBB gene has been rejoined as a target gene. Claims 1-8 were previously canceled. Claims 19-20, 22-25 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected inventions, there being no allowable generic or linking claim. 12-151-10 AIA 12-51-10 Claim s 9 and 17 have been amended in order to correct antecedent basis issues. Claims 14-16 have been canceled. Claims 9-13, 17-18, and 21 are examined on the merits. Priority The present application is a 35 U.S.C. 371 national stage filing of the International Application No. PCT/US2020/062166, filed on November 25, 2020. The instant application claims priority under 35 35 U.S.C. 119(e) or under 35 U.S.C. 120, 121, 365(c), or 386(c) to provisional application 62/941334 filed on November 27, 2019. Information Disclosure Statement The information disclosure statements (IDS) submitted on January 11, 2023; December 21, 2023; March 19, 2024; December 18, 2024; and September 2, 2025 are in compliance with the provisions of 37 CFR 1.97 and have been considered by the examiner. 06-49-06 AIA The listing of references in the specification 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. Maintained Claim Rejections - 35 USC § 103 07-21-aia AIA Claim s 9-13, 18, and 21 are rejected under 35 U.S.C. 103 as being unpatentable over Tak et al. (WO 2018195540A1, found in IDS dated 1/11/2023, hereafter “Tak” and Zhang et al. (US 20160208243 A1, found in IDS dated 1/11/2023, hereafter “Zhang”) . With regard to claim 9 , Tak teaches a transcriptional activator platform (Pg. 1, lines 20-21) comprising a fusion protein that includes a catalytically inactive Cpf1 fused to at least one activation domain (Pg. 1-2, lines 24-27 and 1) wherein the activation domain can include p65 (Pg. 2, line 4) as well as fusion proteins including a catalytically inactive Cpf1 fused to a conditional dimerization domain (Pg. 2, lines 6-8). Tak teaches a second fusion protein comprising at least one activation domain fused to a second dimerization domain (Pg. 2, lines 11-12) and wherein one fusion protein comprises DmrA and one fusion proteins comprises DmrC (Pg. 2, lines, 16-19). Additionally, Tak teaches methods for increasing expression of a target gene comprising use of a first fusion protein including a catalytically inactive Cpf1 fused to a conditional dimerization domain (Pg. 2, lines 32-33) and a second fusion protein comprising an activation domain, which is considered to reasonably read on a gene expression modulating domain, fused to a second conditional dimerization domain and at least one crRNA, which is considered to reasonably read on a gRNA or a plurality of gRNAs, that directs the fusion protein to a regulatory region of a target gene (Pg. 3, lines 1-7, also Fig. 1D). Tak also teaches an embodiment using a nucleic acid which encodes a plurality of gRNAs that direct the fusion protein to a regulatory region, such as a promoter region, of one of the target genes (Pg. 3, lines 21-23) and Pg. 19, line 24). Although Tak provides the specific example of a target gene promoter region (Pg. 2, line 31), it would be known to one having ordinary skill in the art that enhancer regions serve as regulatory regions of genes. Further, Tak teaches that systems using catalytically inactive Cas9 are well known in the art (Pg. 6, lines 18-24) and that the taught fusion proteins can be used in addition to Cas9 proteins which are known in the art (Pg. 15, line 8-9). While Tak teaches use of a plurality of gRNAs targeting a promoter sequence, Tak does not teach use of gRNAs to target both a target gene enhancer sequence in addition to the target gene promoter sequence. Zhang teaches use of a system for the control of gene expression using CRISPR components such as Cas9 and Cpf1 (Para. [0011], lines 3-4) including dead-Cas (Para. [0811], line 5) or dead-Cpf1 (Para. [1028], line 1) and crRNA or gRNA which comprises a sequence complementary to a target nucleic acid sequence which allows for targeting and binding to a desired nucleic acid sequence (Para. [0200], lines 1-4). Additionally, Zhang teaches an inducible CRISPR-Cas system comprising a first fusion construct attached to a first heterodimer and a second fusion construct attached to a second half of the inducible heterodimer an wherein an “inducer energy source” induces dimerization allowing for a functional CRISPR-Cas system comprising a gRNA which targets a specific genetic sequence (Para. [0488]). Zhang also teaches wherein the CRISPR-Cas system may comprise a transcriptional effector domain, which is considered to reasonably read on a gene expression modulating domain, which may be p65 (Para. [0602], lines 5-6) . Further, Zhang teaches a preferred embodiment wherein the system is used to target regulatory control elements such as enhancers in addition to a promoter in order to modify the gene of interest (Para. [1025]). Therefore, it would have been obvious to one having ordinary skill in the art before the effective filing date of the claimed invention, to apply the preferred embodiment of Zhang wherein a CRISPR system is used to target both an enhancer sequence and a promoter sequence to the transcriptional activator platform comprising a first fusion protein including a catalytically inactive Cpf1 fused to a conditional dimerization domain and a second fusion protein comprising an activation domain fused to a second conditional dimerization domain and at least one crRNA that directs the fusion protein to a regulatory region of a target gene as taught by Tak with a reasonable expectation of success. As Tak teaches wherein a plurality of crRNAs can be used which each direct a fusion protein to a regulatory region of a gene (Pg. 3, lines 21-23), a skilled artisan could have easily conceived of use of a plurality of gRNAs comprising different sequences within a target regulatory sequence. One having ordinary skill in the art would have been motivated to make this combination as they would have recognized that targeting both the enhancer and promoter sequence would lead to increased transcriptional regulation of the target gene and therefore more effective modulation of the gene by the transcription activation system. With regard to claim 10 , Tak teaches wherein one fusion protein comprises DmrA and one fusion proteins comprises DmrC (Pg. 2, lines, 16-19). With regard to claim 11 , Tak teaches wherein the conditional dimerization domains dimerize in the presence of a dimerizing agent (Pg. 2, line 14). With regard to claims 12 and 13 , Tak teaches that the activation domain can be p65 (Pg. 2, line 4) which is considered to reasonably read on a protein that directly or indirectly recruits other proteins in the cell that can modulate gene expression. With regard to claim 18 , as detailed above, Tak teaches working embodiments wherein the system can be used to target the HBB gene. With regard to claim 21 , as detailed above, the combined teachings of Tak and Zhang teach a transcriptional activator system comprising a catalytically inactive Cas9 or Cpf1 fused to a conditional dimerization domain and a second fusion protein comprising an activation domain fused to a second conditional dimerization domain and at least one crRNA that directs the fusion protein to a regulatory region of a target gene wherein both the enhancer sequence and promoter sequence of a target gene are targeted. Tak does not teach a pharmaceutical composition comprising the transcriptional activator system and a pharmaceutically acceptable carrier. Zhang teaches wherein the CRISPR-Cas system can be delivered using a dosage of a vector (Para. [0648]) comprising a pharmaceutically-acceptable carrier (Para. [0649], lines 4-5) or via use of lipidoid compounds which can be optionally combined with a pharmaceutical excipient to form a pharmaceutical composition (Para. [0712], lines 1-4 and 14-16). Therefore, it would have been obvious to one having ordinary skill in the art, before the effective filing date of the claimed invention, to apply the use of a pharmaceutical composition comprising a pharmaceutically acceptable carrier in order to deliver the CRISPR-Cas system which can be used for gene editing as taught by Zhang to the transcriptional activator system comprising a catalytically inactive Cas9 or Cpf1 fused to a conditional dimerization domain and a second fusion protein comprising an activation domain fused to a second conditional dimerization domain and at least one crRNA that directs the fusion protein to a regulatory region of a target gene wherein both the enhancer sequence and promoter sequence of a target gene are targeted as taught by the combined teachings of Tak and Zhang with a reasonable expectation of success. As both Tak and Zhang teach wherein CRISPR-Cas based systems can be used to modulate target gene expression of specific genes and Zhang teaches wherein the system can be delivered as a gene therapy-based therapeutic treatment (Para. [0032], lines 5-7), a skilled artisan would be motivated to make this combination in order to create a therapeutic agent having increased gene targeting ability due to the targeting of both the enhancer and promoter regions of a target gene, which would arguably increase effectiveness . Response to Arguments 07-37 AIA Applicant's arguments filed March 2, 2026 have been fully considered but they are not persuasive. With regard to Applicant’s arguments in response to the rejection of claims 9-15, 18, and 21 under 35 U.S.C. 103 over Tak and Zhang, Applicant traverses in section A that the cited art fails to establish a prima facie case of obviousness based on Applicant’s assertion that neither Tak nor Zhang nor the combination “teach the use of two fusion proteins and gRNAs to target both a target gene enhancer sequence in addition to a target gene promoter sequence”. Applicant asserts that Zhang is aimed at characterization of Cpf1 enzymes and that there is nothing in Zhang that would lead a skilled practitioner to the present claims requiring two fusion proteins and gRNAs to target both a gene enhancer sequence in addition to a gene promoter sequence. Applicant concedes that Para. [1025] of Zhang states that the invention “can be used to target endogenous control elements (including enhancers and silencers in addition to targeting of the promoter”, but traverses that it is unclear whether this “means targeting of enhancers or promoters or if it means targeting them at the same time.” Applicant further asserts that, at most, “the combination of references relied upon by the Office establishes that the prior art may have suggested areas for further exploration” but that Zhang does not teach that the presently claimed system would work with a reasonable expectation of success. Applicant further asserts that the Office has cited different features of the present claims from portions of prior art references and thus, relied on impermissible hindsight reconstruction. Applicant’s traversal has been fully considered but is not persuasive. Applicant has canceled claims 14 and 15, thus rendering the rejection of claims 14-15 moot. With regard to Applicant’s traversal that Zhang’s teaching of targeting of enhancers in addition to promoters merely provides areas for further exploration, one of ordinary skill would have easily been able to envision, based on Zhang’s teaching that regulatory control elements can be targeted in addition to a promoter, targeting of both a target gene promoter and target gene enhancer via gRNAs. Applicant is reminded that the MPEP 2123 (I) states that patents are relevant as prior art for all they contain, and that a reference may be relied upon for all that it would have reasonably suggested to one having ordinary skill the art, including nonpreferred embodiments. In instant case, Para. [0198] of Zhang provides examples of well-known regulatory elements including the LTR promoter optionally with the RSV enhancer and the CMV promoter optionally with the CMV enhancer. Since it would be well known to those having ordinary skill in the art that use of the CMV promoter with the CMV enhancer is able to increase transcription, a skilled artisan would have every reason to expect that use of gRNAs targeting an enhancer in addition to one or more promoters would have resulted in the increased gene transcription, especially given Tak’s teaching that gRNAs targeting different promoters were able to synergistically increase target gene expression (See Fig 2G). “The use of patents as references is not limited to what the patentees describe as their own inventions or to the problems with which they are concerned. They are part of the literature of the art, relevant for all they contain.” In re Heck , 699 F.2d 1331, 1332-33, 216 USPQ 1038, 1039 (Fed. Cir. 1983) (quoting In re Lemelson , 397 F.2d 1006, 1009, 158 USPQ 275, 277 (CCPA 1968)). A reference may be relied upon for all that it would have reasonably suggested to one having ordinary skill the art, including nonpreferred embodiments. Merck & Co. v. Biocraft Laboratories , 874 F.2d 804, 10 USPQ2d 1843 (Fed. Cir.), cert. denied, 493 U.S. 975 (1989). In response to applicant's argument that the examiner's conclusion of obviousness is based upon improper hindsight reasoning, it must be recognized that any judgment on obviousness is in a sense necessarily a reconstruction based upon hindsight reasoning. But so long as it takes into account only knowledge which was within the level of ordinary skill at the time the claimed invention was made, and does not include knowledge gleaned only from the applicant's disclosure, such a reconstruction is proper. See In re McLaughlin , 443 F.2d 1392, 170 USPQ 209 (CCPA 1971). In the instant case, the aTF system comprising a first fusion protein comprising catalytically inactive Cas9/Cpf1 and a first dimerization domain, a second fusion protein comprising a gene expression modulating domain and a second dimerization domain, and a plurality of gRNAs comprising different sequences complementary to promoters of the target gene is known based on the teachings of Tak. Targeting of both enhancer and promoter sequences is readily envisioned based on the teachings of Zhang and activation of both enhancer and promoter sequences is well known to be able to increase transcription. Therefore, it would have been predictably obvious one of ordinary skill in the art to modify the aTF system as taught by Tak to include a gRNA targeting an enhancer sequence based on the teachings of Zhang. In regard to the reasonable expectation of success, first, Arguments of counsel cannot take the place of factually supported objective evidence in the record. See In re Schulze , 346 F.2d 500, 602, 145 USPQ 716, 718 (CCPA 1965), In re Huang , 100 F.3d 135, 139-40, 40 USPQ2d 1685, 1689 (Fed. Cir. 1996); In re De Blauwe , 736 F.2d 699, 705, 222 USPQ 191, 196 (Fed. Cir. 1984). Thus, Attorney statements regarding the inoperability of the prior art to target more than one site, are not evidence without a supporting declaration. Second, multiplexed activation via targeting of multiple sites was well known and predictable. Tak teaches use of multiplexed gRNAs in order to synergistically activate gene expression (Pg. 1, 5 th para.; Figs. 2B and 2E; Example 2). Zhang also teaches use of multiplexed gRNAs for targeting of multiple genes (Para. [0840]), See also “Enzymes According to the Invention Used in a Multiplex (Tandem) Targeting Approach, starting at Para. [0835]). Therefore, as use of gRNAs targeting multiple promoters is known to work, one having ordinary skill in the art would have every reason to believe that use of gRNAs targeting both enhancers and promoters would work, especially given Zhang’s suggestion that endogenous control elements (i.e., enhancers) could be targeting via use of the system in addition to the targeting of the promoter. Thus, any conclusions of unpredictability have to be made in the context of this particular in vitro system. Furthermore, the Federal Circuit found that the claims at issue would have been obvious. There had been ample suggestion in the prior art that the claimed method would have worked. Absolute predictability is not a necessary prerequisite to a case of obviousness. Rather, a degree of predictability that one of ordinary skill would have found to be reasonable is sufficient. The Federal Circuit concluded that Applicant’s “[g]ood science and useful contributions do not necessarily result in patentability.” Id. at 1364, 83 USPQ2d at 1304 . 07-22-aia AIA Claim 18 is rejected under 35 U.S.C. 103 as being unpatentable over Tak and Zhang as applied to claim 9 above, and further in view of Lowe et al. (2007, Large-scale genetic fine mapping and genotype-phenotype associations implicate polymorphism in the IL2RA region in type 1 diabetes. Nature genetics , 39 (9), 1074-1082, hereafter “Lowe”) . With regard to claim 18 , as detailed above, the combined teachings of Tak and Zhang teach a transcriptional activator system comprising a catalytically inactive Cas9 or Cpf1 fused to a conditional dimerization domain and a second fusion protein comprising an activation domain fused to a second conditional dimerization domain and at least one crRNA that directs the fusion protein to a regulatory region of a target gene wherein both the enhancer sequence and promoter sequence of a target gene are targeted. Tak teaches working embodiments wherein the system can be used to target the HBB gene. Although Tak teaches wherein the system can be used to target a multitude of clinically relevant human genes such as HBB, AR, and NPY1R genes, Tak does not teach use of the system to target IL2RA. However, Zhang teaches where the CRISPR-Cas system as detailed above can be used to edit chromosomal sequences for a large number of genes including IL2RA (Para. [1449], see Pg. 154, right col., line 15-16). Lowe teaches that development of type-1 diabetes is associated with genetic variants of the IL2RA gene and that genetic variants of the type-1 diabetes associated IL2RA gene are associated with lower levels of circulating IL2RA (Abstract). Lowe additionally teaches an association between the IL2RA gene and autoimmune thyroid disease which suggests a that the IL2RA gene plays a role in some autoimmune diseases (Pg. 1074, 2 nd para.). Therefore, it would have been obvious to one having ordinary skill in the art before the effective filing date of the claimed invention, to apply a CRISPR-Cas transcriptional activation system comprising a first fusion protein fused to a conditional dimerization domain and a second fusion protein comprising an activation domain fused to a second conditional dimerization domain and at least one crRNA that directs the fusion protein to a regulatory sequence of a target gene and wherein both enhancer and promoter target sequences can be targeted as taught by the combined teachings of Tak and Zhang to target the IL2RA gene as taught by Lowe with a reasonable expectation of success. As Zhang teaches targeting of the IL2RA gene by CRISPR-Cas transcriptional activation systems and Lowe teaches that the IL2RA gene is associated with autoimmune diseases such as type-1 diabetes, a skilled artisan would have been motivated to make this combination in order to use the CRISPR-Cas transcriptional activation system in order to treat autoimmune diseases such as type-1 diabetes . Response to Arguments 07-37 AIA Applicant's arguments filed March 2, 2026 have been fully considered but they are not persuasive. With regard to Applicant’s arguments in response to the rejection of claim 18 under 35 U.S.C. 103 over Tak and Zhang in further view of Lowe, Applicant traverses in section B that neither Tak nor Zhang, alone or in combination, render claim 9 and claims depending from claim 9 obvious and that Lowe is cited purely for its disclosure pertaining to IL2RA and therefore fails to cure the deficiencies of Tak and Zhang. Thus, Applicant traverses that one of ordinary skill in the art would not have arrived at the instant invention based on the combination of Tak, Zhang, and Lowe. Applicant’s traversal has been fully considered but is not persuasive. As detailed in the response to the rejections of claim 9 above, the combination of Tak and Zhang is considered to render claim 9 obvious. Tak discloses use of an aTF system to target several genes, the combination of Tak and Zhang teach use of gRNAs targeting both a promoter and enhancer, and Zhang and Lowe teach targeting of IL2RA. Thus, it would have been obvious to a skilled artisan to select IL2RA as the target gene in the aTF system as taught by the combination of Tak and Zhang . 07-22-aia AIA Claim 17 is rejected under 35 U.S.C. 103 as being unpatentable over Tak and Zhang as applied to claim 9 above, and further in view of Matharu et al. (2019, CRISPR-mediated activation of a promoter or enhancer rescues obesity caused by haploinsufficiency. Science , 363 (6424), found in IDS dated 1/11/2023, hereafter “Matharu”) . Claim 17 recites wherein the target gene enhancer or promoter sequences comprises “two or more alleles” and wherein the gRNAs are specific for a subset of the alleles. This is interpreted to be limiting to all diploid cells which necessarily comprise two alleles. With regard to claim 17 , the combined teachings of Tak and Zhang are detailed above and incorporated herein. Tak and Zhang do not teach a transcription activating system comprising gRNA which target a subset of the alleles of a target gene enhancer sequence or a target gene promoter sequence. Matharu teaches use of CRISPR-mediated activation to target the promoter or enhancer of the functional copy of a haploinsufficient gene, which is considered to reasonably read on promoter or enhancer sequences comprising two or more alleles and wherein targeting is to a subset of the two or more alleles (Abstract, see also Fig on Research Article Summary page). Matharu teaches wherein use of a dCas9 fused to transcriptional activator and specific sgRNAs designed to target either the Sim1 promoter or Sim1 enhancer (i.e. SCE2) was able to rescue the obesity phenotype in a heterozygous Sim mouse model (Pg. 2, left col., 1 st para. and 2 nd para.). Therefore, it would have been obvious to one having ordinary skill in the art, before the effective filing date of the claimed invention, to apply the teachings of Matharu wherein gRNAs specific to the promoter or enhancer of a single allele of a gene along with a dCas9 fused to a transcriptional activator were able to target a haploinsufficient gene to the transcriptional activator system comprising a catalytically inactive Cas9 or Cpf1 fused to a conditional dimerization domain and a second fusion protein comprising an activation domain fused to a second conditional dimerization domain and at least one crRNA that directs the fusion protein to a regulatory region of a target gene wherein both the enhancer sequence and promoter sequence of a target gene are targeted as taught by the combined teachings of Tak and Zhang with a reasonable expectation of success. Matharu teaches that over 660 genes are currently thought to cause diseases due to haploinsufficiency (Pg. 1, left col. 1 st para.) and Tak teaches that use of a inducible conditional activator system allows for the transcriptional activator system to be turned on or off via use of a drug (Pg. 7, lines 19-20). Thus, a skilled artisan would have been motivated to make this combination in order to generate a therapeutic system which was able to target a myriad of diseases due to haploinsufficiency by increasing transcriptional activation of a gene wherein the transcriptional activation was controllable via use of a drug, which would lead to the ability to more carefully fine-tune therapeutic treatment . Response to Arguments 07-37 AIA Applicant's arguments filed March 2, 2026 have been fully considered but they are not persuasive. With regard to Applicant’s arguments in response to the rejection of claims 16 and 17 under 35 U.S.C. 103 over Tak and Zhang in further view of Matharu, Applicant traverses in section C that neither Tak nor Zhang, alone or in combination, render claim 9 and claims depending from claim 9 obvious and that Matharu is cited purely for its disclosure pertaining to gRNAs and therefore fails to cure the deficiencies of Tak and Zhang. Thus, Applicant traverses that one of ordinary skill in the art would not have arrived at the instant invention based on the combination of Tak, Zhang, and Matharu. Applicant’s traversal has been fully considered but is not persuasive. Applicant has canceled claim 16, thus rendering the rejection of claim 16 moot. As detailed in the response to the rejections of claim 9 above, the combination of Tak and Zhang is considered to render claim 9 obvious. Tak discloses use of an aTF system to target several genes, the combination of Tak and Zhang teach use of gRNAs targeting both a promoter and enhancer, and Matharu teaches use of a gRNA targeting of a subset of promoters/enhancers diploid cells comprising two alleles. Thus, it would have been obvious to a skilled artisan to use gRNA which are specific for a subset of promoters/enhancers when the promoter/enhancer comprises two alleles in the aTF system as taught by the combination of Tak and Zhang. Citation of Relevant Prior Art 07-96 AIA The prior art made of record and not relied upon is considered pertinent to applicant's disclosure. Ahituv et al. (US 2019/0351074 A1, found in IDS dated 1/11/2023) teaches use of a transcriptional activator system comprising dCas9/gRNA complex targeted to the promoter or enhancer region of a gene (Para. [0006], lines 4-7) which can be used to treat haploinsufficiency (Para. [0007], line 2). Ahituv teaches wherein a catalytically inactive CRISPR comprises a transcriptional activation domain (Para. [0010]) and an embodiment wherein the transcriptional activator domain is used with gRNAs specific for the promoter or enhancer regions of Sim1 and used to target the functional allele of the Sim1 gene in a heterozygous mouse (Paras. [0021], [0022], and [0023]) . Conclusion 07-39 AIA THIS ACTION IS MADE FINAL. Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a). A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action. Any inquiry concerning this communication or earlier communications from the examiner should be directed to ERIN V PAULUS whose telephone number is (571)272-6301. The examiner can normally be reached Mon-Fri 8 AM-5 PM. 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, Doug Schultz can be reached at 571-272-0763. 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. /ERIN V PAULUS/Examiner, Art Unit 1631 /ARTHUR S LEONARD/Examiner, Art Unit 1631 Application/Control Number: 17/779,372 Page 2 Art Unit: 1631 Application/Control Number: 17/779,372 Page 3 Art Unit: 1631
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