The secondary EGFR T790M mutation accounts for about half of acquired resistance mechanisms.1 As a bypass pathway, c‐Met activation caused by c‐Met gene amplification, mutation and/or its ligand hepatocyte growth factor (HGF) overexpression has been reported as another important mechanism in this process.2 In particular, HGF overexpression was observed in about 61% of patients with acquired resistance.3 Therefore, targeting HGF/c‐Met pathway is important for more effective targeted therapy in lung cancer. The gene discussed is EGFR; the disease is lung cancer.