Here, in AML BPCs, we demonstrate for the first time that treatment with the BETi ABBV-075 reduces MCL1 and Bcl-xL levels, while inducing BIM levels, thereby increasing activated BAX and/or BAK levels and undermining the role of MCL1 and Bcl-xL in mediating resistance to venetoclax-induced apoptosis (Fig. 7). The gene discussed is BCL2L11; the disease is acute myeloid leukemia.