Lung cancer is the most fatal malignant tumor worldwide,with non-small cell lung cancer(NSCLC)being the predominant pathological subtype.The development of NSCLC is driven by mutations in the epidermal growth factor receptor(EGFR),and EGFR tyrosine kinase inhibitors(EGFR-TKIs)are employed as targeted therapies for first-line treatment of advanced NSCLC patients harboring EGFR mutations.However,varia-tions in molecular structures,concurrent mutations,and mechanisms of therapeutic resistance contribute to prog-nostic disparities among different EGFR subgroups.This review primarily summarizes the molecular structural basis and differential treatment responses associated with distinct types of EGFR mutations in NSCLC.