Unc-51-like kinase 1 (ULK1)-mediated autophagy activation can control and delay the AML1-ETO9a-driven leukemogenesis in a caspase-3 knockout mouse model of AML [91], suggesting that crosstalk between apoptosis and autophagy determines the pace of AML1-ETO-driven leukemogenesis. Here, CASP3 is linked to acute myeloid leukemia.