In EGFR-mutated lung cancers harboring MET amplification-mediated resistance to EGFR TKIs (which occurs in 10–15% of patients relapsing on first-line third-generation EGFR inhibitors)17,18, various combinations of EGFR and MET TKIs have demonstrated clinical activity and tolerability in phase I/II clinical trials19,20, attesting to the actionability on this resistance driver. The gene discussed is MET; the disease is lung cancer.