Acquired resistance of NSCLC patients to EGFR TKIs treatment is exerted not only through EGFR-dependent mechanisms, but also through molecular alterations in other genes, such as MET and ERBB2 amplifications, PI3KCA, BRAF, and KRAS mutations, and through phenotypic change, such as small cell lung cancer (SCLC) transformation [75,76]. This evidence concerns the gene MET and non-small cell lung carcinoma.