It was discovered that, except for EGFR mutations that account for acquired EGFR-TKIs resistance in NSCLC, aberrant signal pathways or key oncogene-driven genes [19, 20], such as STAT3 activation [9], MET amplification [9, 21] and the transformation of phenotype, including EMT also linked to the TKIs drug resistance [9, 22, 23]. This evidence concerns the gene MET and non-small cell lung carcinoma.