Consequently, the inhibition of MET alone does not effectively suppress the Wnt/β‐catenin signaling pathway in this case, thereby providing a reasonable explanation as to why the combined treatment of EGFR‐TKIs and MET‐TKIs is unsatisfactory against acquired resistance attributed to MET amplification in patients with EGFR‐mutant NSCLC. Here, EGFR is linked to non-small cell lung carcinoma.