Referring to the mechanisms of MET amplification in TKI-resistant tumors, it was acknowledged that MET amplification was pre-existed at low frequencies in untreated HCC827 cells and NSCLC patients (approximately 4%) [26], and under the subsequently drug-selective pressure, these cells appeared to be the dominant clones holding MET amplification and led to clinical gefitinib or erlotinib resistance [27]. This evidence concerns the gene MET and non-small cell lung carcinoma.