BCL2 and acute myeloid leukemia: Recent advancements in AML treatment have identified B‐cell lymphoma 2 (BCL‐2) as a key anti‐apoptotic protein essential for AML cell survival by inhibiting intrinsic apoptosis.[6] BCL‐2 inhibition targets oxidative phosphorylation, selectively eliminating quiescent leukemia stem cells (LSCs) with low oxidative states (ROS‐low) and BCL‐2 overexpression.[7] These LSCs, resistant to conventional chemotherapy, can be effectively targeted by BCL‐2 inhibitors, reducing leukemia burden and improving treatment outcomes.