This was undertaken because, by inhibiting the BET protein BRD4 activity and enhancer-driven expression of several AML relevant oncoproteins, e.g., MYC, CDK4/6 and BCL2, BET protein inhibitors were demonstrated to induce loss of viability in AML with MLL1-r or mtNPM1, and because BRD4 also transcriptionally regulates enhancer-driven expression of HOXA9-MEIS1 and their targets [20, 28–30]. Here, KMT2A is linked to acute myeloid leukemia.