In AML cell lines with AML1/ETO fusion protein, the miR-193a is down-regulated, and treatment of a leukemia mouse model with synthetic miR-193a results in significant tumor regression and reduction of AML1/ETO, CCND1, MDM2 as well as concomitant up-regulation of phosphatase and tensin homolog (PTEN) [85]. The gene discussed is RUNX1; the disease is neoplasm.