Increased activity of MET has been previously reported to mediate resistance to EGFR inhibitors (e.g. osimertinib) in non-small cell lung cancer via EGFR-independent phosphorylation of HER3 and PI3K/Akt activation, providing a bypass pathway in the presence of an EGFR inhibitor (55). The gene discussed is AKT1; the disease is non-small cell lung carcinoma.