MET amplification was observed in 21% of patients with acquired resistance to EGFR TKI (in only 3% of untreated patients) and developed resistance to gefitinib by driving HER3-dependent activation of PI3K in a gefitinib-sensitive lung cancer cell line (HCC827) (6, 7), as well as by activating STAT3 transcription factor directly, through an SH2 domain (51). This evidence concerns the gene MET and lung carcinoma.