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We describe how CSH71, which binds to both the LBD and the ATP\u2010binding pocket of p38\u03b3, is selectively cytotoxic to CTCL Hut78 cells but spares normal healthy peripheral blood mononuclear (PBMC) cells, and propose possible molecular mechanisms for its action. p38\u03b3 is a key player in CTCL development, and we expect that the ability to regulate its expression by specifically targeting the lipid\u2010binding domain will have important clinical relevance. Our findings characterize novel mechanisms of gene regulation in T lymphoma cells and validate the use of computational screening techniques to identify inhibitors for therapeutic development.<\/jats:p>","DOI":"10.1002\/1873-3468.14186","type":"journal-article","created":{"date-parts":[[2021,8,29]],"date-time":"2021-08-29T02:36:40Z","timestamp":1630204600000},"page":"2570-2592","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Targeting the non\u2010ATP\u2010binding pocket of the MAP kinase p38\u03b3 mediates a novel mechanism of cytotoxicity in cutaneous T\u2010cell lymphoma (CTCL)"],"prefix":"10.1002","volume":"595","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9638-0463","authenticated-orcid":false,"given":"Xu Hannah","family":"Zhang","sequence":"first","affiliation":[{"name":"Beckman Research Institute of City of Hope Duarte CA 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