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DEK is a nuclear factor with multifunctional roles, including gene regulation, while its fusion partner, NUP214, plays a pivotal role in nuclear export by interacting with transport receptors such as XPO1. However, the precise mechanism by which DEK::NUP214 drives leukemia remains unclear. A comprehensive multi-omics comparison of 57 AML primary samples (including whole genome sequencing, targeted sequencing, transcriptomics, and drug screening with &gt;500 compounds) revealed that t(6;9) cases display a selective response to XPO1 inhibitors (Selinexor &amp; Eltanexor) and a distinct transcriptomic signature characterized by the overexpression of\n                    <jats:italic>FOXC1<\/jats:italic>\n                    and\n                    <jats:italic>HOX<\/jats:italic>\n                    genes that are key leukemia mediators. CUT&amp;RUN experiments demonstrated the direct binding of DEK::NUP214 to the promoters of\n                    <jats:italic>FOXC1<\/jats:italic>\n                    and\n                    <jats:italic>HOXA\/B<\/jats:italic>\n                    clusters. Strikingly, the expression of these genes and the binding of DEK::NUP214 to their regulatory regions were selectively reduced upon XPO1 inhibition in t(6;9) cells. Altogether, these results identified a novel function of DEK::NUP214 as an XPO1-dependent transcriptional activator of key leukemia drivers and provide a rationale to explore the use of XPO1 inhibitors in this patient population.\n                  <\/jats:p>","DOI":"10.1038\/s41375-025-02593-8","type":"journal-article","created":{"date-parts":[[2025,4,9]],"date-time":"2025-04-09T08:53:06Z","timestamp":1744188786000},"page":"1526-1531","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["DEK::NUP214 acts as an XPO1-dependent transcriptional activator of essential leukemia 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