Secondary EGFR T790M and MET amplification may together account for 70% of this resistance, and activation of the MET/HGF axis, leading to the acquisition of an epithelial-to-mesenchymal transition (EMT) signature, and transformation from NSCLC into small cell lung cancer have also been reported as possible mechanisms of acquired resistance to EGFR-TKIs in NSCLC6, 7, 8, 9, 10, 11. This evidence concerns the gene EGFR and non-small cell lung carcinoma.