As MET amplification is an established mechanism and EGFR and ERBB2 amplification are proposed mechanisms of resistance to tyrosine kinase inhibitor (TKI) therapy in EGFR-mutated NSCLC (38–40), it would be advisable for laboratories to include an ancillary or secondary mechanism of detection of CNVs for samples of EGFR-mutated NSCLC (25). Here, MET is linked to non-small cell lung carcinoma.