Increased level of apoptogenic aldehydes such as methional, malondialdehyde (MDA) and 4‐hydroxynonenal (HNE) can cause damages and senescence in bonne marrow microenvironment and could lead to senescence of normal progenitor, conferring an advantage to ALDH1A1‐overexpressing AML, which will survive in switching from their inflammatory state to reactivate DNA repair.11 This evidence concerns the gene ALDH1A1 and acute myeloid leukemia.