Activation of FLT3 results in elevated tyrosine phosphorylation of LYN and SRC, and inhibitors targeting the SRC family kinases significantly reduced cell viability in FLT3-ITD-dependent AML cell lines, suggesting that the function of SRC family kinases is required for FLT3-induced cell survival37,38. The gene discussed is LYN; the disease is acute myeloid leukemia.