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As a multifaceted cytoskeletal protein, K17 regulates a myriad of biological processes, including cell proliferation and growth, skin inflammation and hair follicle cycling. Aberrant overexpression of K17 is found in various diseases ranging from psoriasis to malignancies such as breast, cervical, oral squamous and gastric carcinomas. Moreover, genetic mutation in <jats:italic>KRT17<\/jats:italic> is related to tissue\u2010specific diseases, represented by steatocystoma multiplex and pachyonychia congenita. In this review, we summarize our findings concerning the regulatory mechanisms of K17 overexpression in psoriasis and compare them to the literature relating to other diseases. We discuss data that proinflammatory cytokines, including interleukin\u201017 (IL\u201017), IL\u201022, interferon\u2010gamma (IFN\u2010\u03b3), transforming growth factor\u2010beta (TGF\u2010\u03b2) and transcription factors glioma\u2010associated oncogene homolog 1\/2 (Gli1\/2), Nrf2 and p53 can regulate K17 by transcriptional and translational control. Moreover, post\u2010translational modification, including phosphorylation and ubiquitination, is involved in the regulation of K17 stability and biological functions. We therefore review the current understanding of the K17 regulatory mechanism and its pathogenic role in diseases from dermatoses to cancer. Prospects for anti\u2010K17 therapy in diagnosis, prognosis and disease treatment are also discussed. Copyright \u00a9 2018 Pathological Society of Great Britain and Ireland. 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