The most common FLT3 mutation in AML is an internal tandem duplication (FLT3-ITD) which involves 3 to 400 base pairs located in the juxtamembrane domain of the receptor leading to receptor dimerization that is independent of receptor binding to the FLT3 ligand (FL; refs. 5–7). This evidence concerns the gene FLT3 and acute myeloid leukemia.