In the case of EGFR TKIs (e.g., gefitinib, erlotinib, afatinib and osimertinib), which have dramatically changed the treatment landscape for patients with EGFR-mutant NSCLC, treatment resistance occurs through on-target and/or bypass resistance mechanisms, the latter of which include HER3-mediated bypass activation in the context of a MET amplification120,125. This evidence concerns the gene ERBB3 and non-small cell lung carcinoma.