Preclinical models have demonstrated that MET-amplification promotes proliferation and survival of EGFR-mutant, TKI-treated NSCLC cells by activating both the MAPK and PI3K/AKT signaling as well as inhibiting the proapoptotic proteins BIM and APAF-1 [137,138,139]. The gene discussed is EGFR; the disease is non-small cell lung carcinoma.