Unlike to these studies performed with human cell lines, others have tracked genetic vulnerabilities in mouse AML cell lines, identifying not only well-defined genes involved in leukemogenesis (Kras, Nras, Bcl2l1, Jak1, Jak2, Brd4 and Brd9), but also potentially actionable targets such as Dcps. Since this gene interacts with components of the spliceosomes, its inhibition could be particularly sensitive in AML patients harboring spliceosome mutations [25]. This evidence concerns the gene BRD4 and acute myeloid leukemia.