Recent work in experimental pancreatitis continues to focus on clarifying pathophysiology and exploring potential therapeutic approaches. Advances in pathophysiology include discovery of a circulating actor involved in colocalization of lysosomal and digestive enzymes in pancreatic acinar cells; characterization of a protein that is increased in expression several hundredfold during the development of acute pancreatitis; identification of glutathione as an endogenous protective factor against pancreatic injury; and implication of microtubule disruption as a major event in cerulein-induced pancreatitis. Studies of potential therapies have failed to resolve outstanding issues concerning the therapeutic benefit of protease inhibitors and cholecystokinin receptor antagonists but suggest that agents that alter microvascular blood flow to the pancreas may affect the severity of injury to the gland.