Investigators employ animal models of pancreatitis for two principal reasons: to answer questions regarding the pathophysiology and cellular biology of the disease and to test novel treatment modalities. The past year has seen progress in both fields. Factors that determine vascular blood flow and coagulation have been the focus of much attention. Premature protease activation, generation of oxygen radicals, and ethanol toxicity have been investigated to characterize further their roles in triggering pathophysiologic events. New models that mimic a gallstone-induced or autoimmune pathogenesis of pancreatitis have emerged or gained ground. The mechanisms involved in pancreatic regeneration remain a subject of ongoing controversy.