A plausible mechanism of beta-blocker therapy in the reduction of pancreatic cancer risk is that by inhibiting beta receptors, it could lead to decreased cyclic adenosine monophosphate (cAMP) signaling, and downregulate cAMP-dependent epidermal growth factor (EGF) and vascular endothelial growth factor (VEGF) production [35,36]. This evidence concerns the gene EGF and familial pancreatic carcinoma.