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Although the JAK1\/2 inhibitor Ruxolitinib is clinically approved, its efficacy is limited by toxicity to normal cells and the development of drug resistance. Here, the deSUMOylase DESI2 is identified as a novel component of the JAK2\u2010V617F complex by mass spectrometry\u2010based proteomics. Mechanistically, DESI2 selectively binds to and stabilizes JAK2\u2010V617F by mediating its deSUMOylation and deubiquitination at lysine 962 (K962). Importantly, DESI2 protein is specifically and highly expressed in JAK2\u2010mutant\u2010driven cell lines and MPN primary clinical samples, suggesting its potential role in JAK2\u2010V617F regulation and disease progression. Genetic depletion of DESI2 suppresses both JAK2 mutant cell growth and MPN disease onset\u00a0in vitro and in vivo. Moreover, through a compound screen, followed by chemical proteomics and compound optimization, WWQ\u201003\u2010012 is discovered, which selectively degrades mutant JAK2, induces primary leukemia cells death, and inhibits MPN progression through targeting DESI2 enzymatic activity\u00a0in vitro\u00a0and\u00a0in vivo. These studies provide a novel therapeutic strategy against mutated JAK2 signaling in MPN and sAML.<\/jats:p>","DOI":"10.1002\/advs.202515127","type":"journal-article","created":{"date-parts":[[2025,12,3]],"date-time":"2025-12-03T09:03:52Z","timestamp":1764752632000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Targeting DESI2 as a Novel Therapeutic Strategy for JAK2\u2010Mutant Leukemias"],"prefix":"10.1002","volume":"13","author":[{"given":"Husheng","family":"Mei","sequence":"first","affiliation":[{"name":"Department of Hematology Tongji Hospital Frontier Science Center for Stem Cell Research Shanghai Key Laboratory of Signaling and Disease Research School of Life Sciences and Technology Tongji University  Shanghai 200092 P. R. 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