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Introduction Management of acute myeloid leukemia (AML) continues to be a therapeutic challenge despite significant recent advancements. Dysregulation of several components of apoptotic pathways has been identified as potential driver in AML. Areas covered Overexpression of anti-apoptotic proteins, B-cell lymphoma 2 (BCL2), BCL-XL, and myeloid cell leukemia-1 (MCL1), has been associated with worse outcome in AML. Dysfunction of p53 pathway (often through mouse double minute 2 homolog (MDM2)) and high expression of inhibitor of apoptosis