Our results revealed that overexpression of miR-376a-3p evidently inhibited the proliferation, arrested in the G0/G1 phase and induced apoptosis of AML cells, and its suppressive effect could be reversed when MT1X was overexpressed, which were consistent with the trend of miR-376a-3p effects in other tumors. The gene discussed is MT1X; the disease is acute myeloid leukemia.