EGFR is a transmembrane tyrosine kinase receptor belonging to the ErbB family that regulates critical cellular processes including proliferation, differentiation, and survival 1. Upon ligand binding, EGFR undergoes autophosphorylation and initiates downstream signaling cascades involving the MAPK and PI3K pathways 2. The receptor's cellular fate is controlled through endocytosis, with internalized EGFR either degraded in lysosomes or recycled to the cell surface 3. EGFR exhibits tissue-specific functions, including regulation of sebaceous lipogenesis where receptor downregulation increases lipid accumulation 4. In glioblastoma, EGFR can paradoxically function as a tumor suppressor when amplified, with ligand abundance determining whether it promotes or inhibits tumor invasion 5. EGFR aberrations drive multiple cancer types through mechanisms including gene amplification, overexpression, and oncogenic mutations 6. In colorectal cancer, EGFR regulates COX-2 expression and cooperates with ErbB-2 in promoting cell survival 7. Resistance to anti-EGFR therapy can arise through HER3 heterodimerization, which reactivates downstream signaling pathways 8. Multiple EGFR-targeted therapies are clinically approved, including tyrosine kinase inhibitors such as afatinib, osimertinib, and amivantamab 9. Atypical EGFR mutations in non-small cell lung cancer show heterogeneous drug sensitivities requiring personalized treatment approaches 10.