Taken together, the ability of SYK and dual FLT3/SYK suppression to enhance the growth inhibitory effects of midostaurin and other FLT3 inhibitors in the context of both kinase inhibitor-sensitive and kinase inhibitor-resistant disease warrants further investigation for the continued development and optimization of midostaurin as a treatment strategy for AML. This evidence concerns the gene FLT3 and acute myeloid leukemia.