RUNX1T1 and acute myeloid leukemia: 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].