In APL, preliminary whole genome/exome studies involving about thirty APL patients identified several somatic mutations affecting up to 135 different genes in a non-recurrent manner, except for FLT3, WT1 and KRAS. These findings suggest that APL is a heterogeneous disease with secondary relevant changes not yet defined [4–8]. The gene discussed is FLT3; the disease is acute promyelocytic leukemia.