MET alterations were involved in several cancers and consisted of MET mutations in renal papillary cancer (1–4%, first described in tumours), as well as MET amplification (MET AMP) in gastric cancer, melanoma (12%), de novo or as resistance to tyrosine kinase inhibitors in epidermal growth factor receptor (EGFR)-mutated NSCLC (15%), or colorectal cancer that develops resistance to EGFR antibodies [12,13,15,16,17]. This evidence concerns the gene EGFR and gastric cancer.