In summary, this study demonstrates that in the case of H2170 EGFR and c-Met TKI-resistant NSCLC cells, which are EGFR wild-type, the canonical Wnt and mTOR pathways have prominent roles in facilitating alternative EGFR/c-Met signaling mechanisms, resulting in the development of TKI resistance and cancer cell survival. The gene discussed is MET; the disease is non-small cell lung carcinoma.