KIT and Ewing sarcoma: These response rates are largely dominated by multi-RTK small molecule inhibitors that combine a strong anti-angiogenic component via inhibition of the vascular endothelial growth factor receptors (VEGFRs) with simultaneous inhibition of other key RTKs implicated in OS and ES progression, including the platelet-derived growth factor receptors (PDGFRs), c-KIT, fibroblast growth factor receptors (FGFRs), RET, and/or MET.