Given that the impact of selective c-MET inhibitor CR on GISTs’ viability was modest, even when combined with IM and taking into the account that CB was much more potent when compared to CR, we concluded that activation of FGFR, but not the MET-signaling, pathway was the major driving component of IM resistance in GIST T-1R cells. Here, MET is linked to gastrointestinal stromal tumor.