Supporting this idea, the chromatin accessibility of AE‐binding sites was revealed to be more preferentially regulated by KDM4B compared to that of native AML1‐binding sites, involving active enhancer marks and functional cis‐regulatory elements, which was observed using a t(8;21)‐derived AML cell model and demonstrated by open chromatin analysis. The gene discussed is RUNX1; the disease is acute myeloid leukemia.