This conference marked the end of an era of uncertainty about mechanisms initiating acute pancreatitis in humans, the validity of various animal models, and the relationship between acute and chronic pancreatitis. It is now clear that active trypsin plays a central role in the initiation of one or more types of acute pancreatitis. It is now possible to identify certain individuals at risk for pancreatitis before the first attack through genetic testing and to distinguish hereditary pancreatitis from other forms of pancreatitis. The importance of identifying the site and mechanism of trypsinogen activation in animal models of acute pancreatitis has also been realized. Furthermore, it is now clear that human chronic pancreatitis can arise from recurrent attacks of acute pancreatitis through the necrosis-fibrosis sequence. The initial presentation of the strikingly high incidence of cystic fibrosis mutations in idiopathic chronic pancreatitis and relapsing acute pancreatitis was unveiled, suggesting another strong genetic predisposition to pancreatitis. Finally, the strong influence of prolonged chronic pancreatitis in the development of pancreatic cancer is now clear. Thus, this conference marked the beginning of an new era of pancreatic research based on molecular mechanisms in humans and it opened the possibility of developing new therapies designed to limit or prevent human suffering from many diseases of the pancreas.