Strikingly, CB treatment also provided a moderate inhibitory effect on FGFR2 phosphorylation in GIST T-1R cells, thus suggesting the novel molecular mechanism responsible for the CB inhibitory effect in IM-resistant GISTs with this type of RTK switch (loss of KIT/gain of FGFR). The gene discussed is FGFR2; the disease is gastrointestinal stromal tumor.