First, although preclinical data have suggested the crosstalk between MET and EGFR [23], the role of MET amplification in the development of resistance to EGFR TKIs has been observed mostly in patients with EGFR mutation [24, 25, 35], not in patients with EGFR wild-type NSCLC. The gene discussed is EGFR; the disease is non-small cell lung carcinoma.