The pathogenesis of pancreatic cancer is significantly influenced by the aberrant expression and persistent activation of various cell surface receptor tyrosine kinases (RTKs), including EGFR (epidermal growth factor receptor), VEGFR (vascular endothelial growth factor receptor), and PDGFR (platelet-derived growth factor receptor), and their downstream oncogenic pathways, contributing to disease initiation, progression and chemoresistance [8–10]. The gene discussed is EGFR; the disease is pancreatic neoplasm.