Because PI3K/AKT-dependent MCL1 expression can promote resistance to the recently approved BCL2 inhibitor venetoclax in patients with AML, simultaneous targeting of anti-apoptotic proteins such as MCL1, BCL2, or BCL2L1 (BCL-xL) and PI3K/AKT signaling might cooperatively boost apoptotic activity in AML cells. Here, BCL2L1 is linked to acute myeloid leukemia.