In fact, mutations involving KIT, FLT3 and RAS were commonly reported in CBF-AML.8, 10, 11, 20 Knock-in mouse models of RUNX1/RUNX1T1 or CBFB/MYH11 induced a preleukemia hematopoietic state and required additional mutations for the development of AML,21, 22 supporting the proposition of a ‘second-hit' leukemogenic model. This evidence concerns the gene RUNX1T1 and acute myeloid leukemia.