Recent studies found different tumors with MET amplification were extraordinarily susceptible to the selective MET tyrosine kinase inhibitor (TKI) [12–14], and MET amplification was responsible for approximately 20% of the acquired resistance to epidermal growth factor receptor (EGFR) TKI treatment in lung adenocarcinomas [15, 16]. This evidence concerns the gene MET and lung adenocarcinoma.