KIT and gastrointestinal stromal tumor: Importantly, FGF-2 used for IM-resistant GISTs (i.e., GIST T-1R and GIST 430) also significantly increased the production of VEGF-A (Supplementary Figure S1), thereby illustrating that FGF2-mediated signaling in GIST might activate the compensatory mechanism of VEGFR activation to maintain cancer cell survival and angiogenesis in GISTs, thereby illustrating that the inhibition of KIT signaling in GISTs might the activate compensatory mechanism of VEGFR activation to maintain cancer cell survival and angiogenesis in GISTs.