AML is a group of heterogeneous disorders associated with distinct genetic aberrations, and the impairment of PU.1 is different in various subtypes, e.g., low expression in acute promyelocytic leukemia (APL) harboring t(15; 17)5, and low activity in AML with t(8; 21)6. This evidence concerns the gene SPI1 and acute myeloid leukemia.