Background Epidermal growth factor receptor (EGFR) gene mutations play a key driving role in the development and progression of lung cancer. Currently, EGFR tyrosine kinase inhibitors (TKIs) serve as the standard first-line therapy for patients with advanced non-small cell lung cancer (NSCLC) harboring EGFR mutations. However, with the widespread use of these drugs, resistance has become increasingly prevalent, particularly with third-generation EGFR-TKIs, posing a significant bottleneck limitin