Taken together, the reported results indicate that co-activation of MET signaling at baseline in EGFRm+ NSCLC is an event that may cause intrinsic resistance to EGFR-TKIs, but at the same time, it may also represent a potential target for first-line combination therapy aimed at disabling the inherent resistance to EGFR inhibition. This evidence concerns the gene MET and non-small cell lung carcinoma.