Consistent with venetoclax mediating BAX/BAK-dependent outer mitochondrial membrane permeabilization (37), respiration of AML cells exposed to venetoclax was increased following the addition of cytochrome C, indicating that BCL-2 inhibition results in permeabilization of the outer mitochondrial membrane [Fig. 4B; compare “FC (3.0 μM)” to “Cyt C”]. Here, BAK1 is linked to acute myeloid leukemia.