Background Lung adenocarcinoma (LUAD) frequently harbors activating mutations in the epidermal growth factor receptor (EGFR), making EGFR tyrosine kinase inhibitors (EGFR-TKIs) a critical component of targeted therapy. Although third-generation EGFR-TKIs, such as Furmonertinib, have improved outcomes for patients with EGFR-mutant LUAD, drug resistance and tumor adaptation remain major challenges. The cellular and molecular mec...