EGFR and neoplasm: This notion is supported by the observations that in gastric cancers, as well as in a smaller subset of lung and esophageal cancers, sensitivity to c-Met small-molecule inhibitors, including crizotinib, is strongly linked to Met gene amplification or receptor overexpression, as in EGFR-positive NSCLC tumours responsiveness to kinase inhibitors correlates with both EGFR and HER2 gene amplification [77,78,79].