reported that MET FISH positivity (HR 2.83, 95% CI 1.37-5.86) was an independent predictor for poorer PFS in patients with EGFR-mutant NSCLC who received first-line EGFR-TKI treatment after adjustment for multiple factors including BIM, ALK, KRAS, PIK3CA, PTEN, MET, etc. Studies on EGFR-TKI-naïve patient-derived xenograft model harboring concurrent EGFR L858R and MET amplification demonstrated partial sensitivity with EGFR-TKI monotherapy but achieved CR with EGFR-TKI combined with crizotinib, suggesting that both EGFR and MET are oncogenic drivers that are sensitive to inhibition.9 The gene discussed is MET; the disease is non-small cell lung carcinoma.