Finally, as mentioned in Section 2.2.3, preclinical models have shown that aberrant MET signaling due to MET-amplification renders EGFRM+ NSCLC cells TKI-resistant by promoting their proliferation and survival via reactivation of the MAPK and PI3K-AKT pathways that are inhibited by EGFR-TKIs [138]. The gene discussed is AKT1; the disease is non-small cell lung carcinoma.