An experimental study demonstrated that signaling crosstalk between c-KIT and FGFR3 activated the MAPK pathway to promote resistance to imatinib, providing a mechanistic rationale to target FGFR3 as a strategy to improve the treatment of GIST patients with de novo or acquired resistance to imatinib [41]. This evidence concerns the gene FGFR3 and gastrointestinal stromal tumor.