Bcl-2/Bcl-XL and Mcl-1 act redundantly as effectors of BMM-mediated AML drug resistance, highlighting the potential of Mcl-1 suppression to reverse BMM-mediated drug resistance in the leukaemic stem cell population, thus preventing disease relapse and ultimately improving patient survival. Suppression of Mcl-1 expression by the CDC7/CDK9 inhibitor PHA-767491 overcomes bone marrow stroma-mediated drug resistance in AML. Here, MCL1 is linked to acute myeloid leukemia.