Activation mutation of upstream regulators such as Fms-like tyrosine kinase 3 (FLT3) and KIT is a frequent event in AML pathogenesis, regulating various downstream pathways such as Ras/Raf/MEK/ERK, PI3K/PTEN/AKT/mTOR, and Jak/STAT and resulting in leukemogenesis [2]. The gene discussed is FLT3; the disease is acute myeloid leukemia.