The treatment of advanced non-small cell lung cancer (NSCLC) with activating mutations in EGFR has evolved significantly over the past 20 years. The basis of treatment are third-generation EGFR tyrosine kinase inhibitors (TKIs), such as osimertinib, used alone or in combination with chemotherapy or the bispecific anti-EGFR MET antibody amivantamab. Repeat tissue biopsies after progression on EGFR TKI reveal targeted genomic and histological changes. These alterations cause resistance to TKIs in a subset of patients. The article focuses on targeting MET-mediated TKI resistance in EGFR-mutant NSCLC.[1][2][5][6]