Notably, of 10 patients with MET-amplified GE cancers, none were included in a crizotinib trial.[12] Preclinical data suggest that MET amplified gastric tumors may be sensitive to c-MET inhibitors.[23] We report disappointing results for the three patients with MET abnormalities included in trials with these agents (1 patient with a MET variant and 2 with MET amplification). This evidence concerns the gene MET and gastric neoplasm.