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). Here, BAK1 is linked to acute myeloid leukemia.