EGFR and lung carcinoma: However, third-generation EGFR-TKI remains a challenge, with resistance mechanisms including EGFR-dependent and non-EGFR-dependent resistance [5, 6], such as the C797S mutation [7, 8], MET amplification [9, 10], HER2 mutation [11], or amplification, etc. In addition to the inevitable acquired resistance, current EGFR-TKIs primarily benefit patients with EGFR-activating mutations, offering limited efficacy for wild-type EGFR (WT-EGFR) lung cancer patients.