Its mutations were also found in about 10% of acute myeloid leukemia (AML) [6], and inhibition of its expression or function is also blocked by leukemogenesis-related genetic alterations such as t(8;21)-generated AML1-ETO [7]–[9] or t(9;22)-generated BCR-ABL fusion protein [10]. This evidence concerns the gene RUNX1 and acute myeloid leukemia.