Specific small molecule inhibitor 9a significantly improves the clinical prognosis of acute myeloid leukemia (AML) by targeting the interaction between NCOA4 and FTH1, leading to depletion of iron content in LIP, thereby inhibiting ferritin autophagy, blocking lipid peroxidation and ferroptosis, and exerting an inhibitory effect on the self-renewal and viability of leukemic stem cells (47, 48). This evidence concerns the gene NCOA4 and acute myeloid leukemia.