Internal tandem duplications (ITDs) in the FMS-like tyrosine kinase 3 (FLT3) gene are among the most common abnormalities seen in younger adult AML and are present in approximately 30% of patients; it leads to constitutive FLT3 kinase activity and downstream activation of signal transducer and activator of transcription 5 (STAT5) [2, 3]. Here, FLT3 is linked to acute myeloid leukemia.