To further elucidate the potential mechanism of TCP1-mediated AML cell survival, we analyzed its regulatory effects on PLK1 (a cell cycle regulator) and AML1-ETO (a leukemia-associated fusion protein) using AML cell lines with constitutive TCP1 knockdown (HL-60-G4-shTCP1 and Kasumi-1-shTCP1). This evidence concerns the gene RUNX1T1 and acute myeloid leukemia.