Given its critical role in normal cellular function, aberrations in MET signaling are considered as one of the oncogenic drivers in the development and progression of lung cancer.6, 7, 8 Aberrations in MET, either amplification or overexpression, have been reported in 2%-8% of EGFR-mutant NSCLCs with no prior exposure to EGFR-TKI therapy.6, 7, 8 Preclinical evidence had demonstrated that the coexistence of EGFR mutation and MET amplification/overexpression in the same tumor reduces sensitivity to EGFR-TKI, which poses challenges to clinical therapy.9 Here, MET is linked to lung cancer.