In AML, a general drop in ALDH1A1 expression in tissue could coincide with the loss of normal progenitor cells; however, AML stem cells overexpressing ALDH1A1 gain an advantage: on the one hand it protects directly from antineoplastic agents, and on the other hand it reactivates DNA repair, by removing toxic aldehydes that inactivate repair enzymes [126]. The gene discussed is ALDH1A1; the disease is acute myeloid leukemia.