In addition to being the major sites for biosynthesis and energy supply, mitochondria initiate apoptotic signalling in AML cells triggered by chemotherapeutic agents, which includes anti‐apoptotic BCL2, BCL‐xL (also termed BCL2L1) and MCL1, and pro‐apoptotic BAX, BAK (BAK1) and cytochrome c, as well as ROS (Indran et al, 2011). This evidence concerns the gene BCL2L1 and acute myeloid leukemia.