Given that IM-resistant GIST T-1R cells overexpressed FGFR2α and MET and taking into account that the RTK switch is a one of the mechanism underlying the IM resistance of GISTs, we further examined whether inhibition of FGFR2a and MET might have a prospective use against the IM-resistant GIST subset with this type of RTK switch. This evidence concerns the gene MET and gastrointestinal stromal tumor.