FLT3 and cancer: Exogenous or autocrine growth factors activating RTKs—such as epidermal growth factor receptor (EGFR), receptor tyrosine-protein kinase erbB-2 (Her2), platelet-derived growth factor receptor (PDGFR), insulin-like growth factor 1 (IGF1-R), vascular endothelial growth factor (VEGFR), fms-like tyrosine kinase 3 (Flt3), and c-Kit—increase the activity of downstream ERK1/2 in many cancers [7].