Internal tandem duplication (ITD), which represents the most commongroup of FLT3 mutations, occurs in 20–25% of all AML patients.ITD promotes ligand-independent dimerization and downstream signaling.6,7 Point mutations in the tyrosine kinase domain (FLT3-TKD) are approximatelytwice less prevalent. This evidence concerns the gene FLT3 and acute myeloid leukemia.