AVP and alcohol abuse: Figure 1 summarizes the take-home message of our current understandings of mechanisms of ethanol-induced pancreatic dysfunction: (i) inhibition of hepatic ADH during chronic alcohol abuse could be a key metabolic event resulting in an increased formation of FAEEs via nonoxidative metabolism in the pancreas that ultimately promotes the pathogenesis of CP; (ii) an adaptive UPR maintains ER homeostasis with alcohol abuse and prevents pancreatitis responses in the acinar cell.