As high Met amplification level is a resistance mechanism to AZD9291, our data demonstrated that AZD9291 increased the expression of Met compared to that of the controls, whereas Met expression was dramatically down‐regulated in the harmine plus AZD9291 combination‐treated NSCLC cells compared to that of monotherapy, indicating that harmine might be an attractive agent to reverse Met overexpression induced by AZD9291. This evidence concerns the gene MET and non-small cell lung carcinoma.