{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,8]],"date-time":"2026-09-08T02:28:49Z","timestamp":1788834529922,"version":"build-2803163510"},"reference-count":38,"publisher":"MDPI AG","issue":"15","license":[{"start":{"date-parts":[[2023,8,1]],"date-time":"2023-08-01T00:00:00Z","timestamp":1690848000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>Understanding the factors creating genetic susceptibility in psoriasis may provide a basis for improving targeted treatment strategies. In this review, we discuss the genes linked to the pathogenesis of psoriasis and their relationship to the available treatment options. To identify the relevant genetic markers and treatments, we searched PubMed, Google Scholar, MEDLINE, and Web of Science with keywords, including genetic susceptibility to psoriasis, genetics\u00a0and\u00a0psoriasis, psoriasis treatments, and biologics\u00a0treatments in psoriasis. The articles in English from database inception to 1\/1\/23 were included. Case reports and series were excluded. Gene variant forms commonly implicated in the pathogenesis of psoriasis include those encoding for interleukins, interferons, and other mediators involved in inflammatory pathways, such as JAK\/STAT, and NF-\u03baB. Several of the treatments for psoriasis (for example IL23 and TYK2 inhibitors) target the products of genes linked to psoriasis. Multiple genes are linked to the pathogenesis of psoriasis. This understanding may provide an avenue for the development of new psoriasis treatment strategies and for more effective, safer treatment outcomes.<\/jats:p>","DOI":"10.3390\/ijms241512310","type":"journal-article","created":{"date-parts":[[2023,8,1]],"date-time":"2023-08-01T09:06:44Z","timestamp":1690880804000},"page":"12310","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["The Genetic Susceptibility to Psoriasis and the Relationship of Linked Genes to Our Treatment Options"],"prefix":"10.3390","volume":"24","author":[{"given":"Heli A.","family":"Patel","sequence":"first","affiliation":[{"name":"Center for Dermatology Research, Wake Forest School of Medicine, Winston-Salem, NC 27104, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3951-2703","authenticated-orcid":false,"given":"Rishab R.","family":"Revankar","sequence":"additional","affiliation":[{"name":"The Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sofia T.","family":"Pedroza","sequence":"additional","affiliation":[{"name":"Baylor College of Medicine, Houston, TX 77030, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shaveonte","family":"Graham","sequence":"additional","affiliation":[{"name":"Wright State University Boonshoft School of Medicine, Fairborn, OH 45435, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0090-6289","authenticated-orcid":false,"given":"Steven R.","family":"Feldman","sequence":"additional","affiliation":[{"name":"Center for Dermatology Research, Wake Forest School of Medicine, Winston-Salem, NC 27104, USA"},{"name":"Department of Dermatology, Wake Forest School of Medicine, Winston-Salem, NC 27104, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2023,8,1]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","unstructured":"Singh, R., Koppu, S., Perche, P.O., and Feldman, S.R. 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