Most strikingly, we observed a significant phosphorylation of FGFR2α in the IM-resistant GIST cells, whereas phosphorylation of KIT and PDGFRα was reduced when compared to IM-sensitive parental GIST cells, thus suggesting the novel type of RTK switch (loss of KIT and gain of FGFR) developed in IM-resistant GIST T1-R cells. This evidence concerns the gene KIT and gastrointestinal stromal tumor.