The disease in the lungs saw significant improvement until the introduction of crizotinib, a prototype type-I MET inhibitor with a U-shaped binding mode at the ATP binding site, which showed tremendous promise in treating non-small cell lung cancer and gastric cancer patients harboring MET amplification.[11–13] Based on that, it was posited that the tumor subgroups in the lungs might be primarily driven by c-Met amplification, rather than Her-2 amplification. This evidence concerns the gene MET and gastric cancer.