Therapy targeting specific somatic mutations has become an increasingly important part of cancer therapy over the past 20 years. In particular, tyrosine kinase inhibitors (TKIs) have become a critical component of treatment for both solid tumors and hematologic malignancies. Since mutations in the FMS-like tyrosine kinase 3 (FLT3) gene are relatively common in acute myeloid leukemia (AML), activating mutations in FLT3 represent an appealing target for drug development. Efforts are well underway to develop FLT3 inhibitors and to incorporate these agents into AML therapy.

 

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