CBF AML is determined by the disruption of CBF signaling by recurrent chromosomal translocations, either t(8;21)(q22;q22), corresponding to the formation of the RUNX1/RUNX1T1 fusion gene (formerly known as AML1/ETO), or inv(16)(p13q22)/t(16;16)(p13q22), producing the aberrant CBFB/MYH11. This evidence concerns the gene RUNX1 and acute myeloid leukemia.