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FMS-like tyrosine kinase 3 (FLT3) is among the most common driver genes recurrently mutated in acute myeloid leukemia (AML), accounting for approximately 30% of cases. Activating mutations of the FLT3 receptor include internal tandem duplications (ITD) that map to the auto-inhibitory juxtamembrane (JM) domain or point mutations within the tyrosine kinase domain (TKD). Several FLT3 tyrosine kinase inhibitors have been developed in the last few years, but midostaurin is currently the only one approved for the treatment of newly diagnosed patients harboring  FLT3  mutations. Here we describe for the first time a novel in-frame deletion in exon 14 (JM domain) of the  FLT3  gene, that we identified in a young woman with CBFb-MYH11-positive AML. We demonstrated that this novel  FLT3  variant is pathogenic, since it is responsible for constitutive activation of FLT3 receptor. Finally,  ex-vivo  studies demonstrated that this novel mutation is sensitive to midostaurin.

Case Report: A Novel Activating FLT3 Mutation in Acute Myeloid Leukemia