Targeted deletion of an upstream regulatory element of the mouse gene Sfpi1 (common human name SPI1) encoding the transcription factor PU.1, a key hematopoietic regulator for myeloid differentiation, results in homozygous PU.1 hypomorphs that develop AML (or much less frequently T-cell lymphomas) after a latency of 3 to 8 months [21,22]. This evidence concerns the gene SPI1 and acute myeloid leukemia.