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). The gene discussed is PLK1; the disease is acute myeloid leukemia.