Finally, to interrogate the molecular mechanisms that underpin the requirement for the cBAF and COMPASS–MLL complexes in Npm1c and Flt3-ITD AML, and how these differ from normal hematopoiesis, we compared the genome-wide binding patterns of Smarcb1 (an exemplar of cBAF), Kmt2a (COMPASS-MLL1) and Kmt2d (COMPASS-MLL4) using ChIP–seq across leukemia, normal myeloid progenitors (GMP) and mature myeloid subsets (Fig. 6a). Here, FLT3 is linked to acute myeloid leukemia.