A receptor tyrosine kinase FMS-like tyrosine kinase-3 (FLT3) [28] is constitutively activated by internal tandem duplications (FLT3/ITD mutations) in approximately 30% of de novo AML patients [29], [30], which is recognized to cause a greater relapse rate and a poorer overall survival in AML patients [29]. Here, FLT3 is linked to acute myeloid leukemia.