Clinically, EGFR is a prognostic marker and an effective therapeutic target of multiple human cancers, especially NSCLC.21 However, it is well known that the EGFR inhibitors widely face primary resistance (~60%) and rapidly generate acquired resistance (6–12 months).22, 23 Therefore, the downstream effector function of EGFR may act as a substitutable therapeutic target of EGFR to overcome the drug resistance.24, 25 The previous study26 showed that EGFR inhibition attenuated liver fibrosis and the development of hepatocellular carcinoma. This evidence concerns the gene EGFR and non-small cell lung carcinoma.