On the molecular level, some investigators have suggested that miR-193a-3p silencing, due to DNA hypermethylation by the AML1/ETO co-repressor complex, would increase the oncogenic activity of the fusion protein AML1/ETO expressed in hematopoietic cells, thereby contributing to leukemogenesis in patients with acute myeloid leukemia [38]. The gene discussed is RUNX1; the disease is acute myeloid leukemia.