“…Because trypsin is one of the oldest known digestive enzymes, and because trypsin can activate several other digestive proteases in the gut and in vitro, and because pancreatitis is regarded as a disease caused by proteolytic autodigestion of the pancreas, it would seem reasonable to assume that pancreatitis is caused by a trypsindependent protease cascade within the pancreas itself. If this hypothesis was correct, the trypsinogen mutations that are found in association with hereditary pancreatitis should confer a gain of enzymatic function [18,19], and mutant trypsinogen would be activated more readily inside acinar cells or, alternatively, active trypsin would be degraded less rapidly inside acinar cells. Both events would lead to a prolonged or increased enzymatic action of trypsin within the cellular environment.…”