MET and non-small cell lung carcinoma: Alterations in MET resulting from either gene amplification or exon 14 skipping have been considered as therapeutic targets in NSCLC and clinically benefit from treatment with crizotinib or other MET-TKIs.21, 22, 23 However, a subset of treatment-naïve NSCLCs would present with concurrent mutations in EGFR and MET,6 which has been implicated in the primary resistance to EGFR-TKI in NSCLC.2