These data, taken together, highlight the relevance of FGF signaling in GISTs devoid of KIT/PDGFRA mutations or RAS-pathway activation, suggesting that FGF4 autocrine loop or FGFR mutations in SDH-deficient and qWT GISTs act as a surrogate of KIT/PDGFRA alterations in sustaining GIST tumor growth and spreading. The gene discussed is KIT; the disease is neoplasm.