Lai GGY, et al. - In view of the implication of mesenchymal epithelial transition factor (MET) activation as an oncogenic driver in epidermal growth factor receptor (EGFR)–mutant non–small-cell lung cancer (NSCLC) and its possible mediation of primary and secondary resistance to EGFR tyrosine kinase inhibitors (TKI), researchers assessed the clinical relevance of MET copy number gain (CNG) in 200 consecutive NSCLC patients identified as metastatic treatment-naïve EGFR-mutant–positive via MET fluorescence in situ hybridization. Outcomes revealed that up to 26% of TKI-naïve EGFR-mutant–positive NSCLC have high MET CNG; this seemed not significantly impact response to TKI, except in patients who were MET-amplified. Adopting arbitrary copy number thresholds was shown to be limiting, and a cross-assay validation seems required to define therapeutically tractable MET pathway dysregulation in EGFR-mutant–positive NSCLC.