The identification of the genetic basis of hereditary pancreatitis in 1996 confirmed the critical role of trypsinogen in this disease and opened a new avenue of research on pancreatitis-associated genetic risk factors and their mechanism of action. Through the following 25 years, the ensuing discoveries fundamentally changed our understanding of pancreatitis pathogenesis, clarified the role of trypsinogen autoactivation in disease onset and progression, and set the stage for future therapeutic interventions. This Frank Brooks Memorial Lecture was delivered on November 4, 2021, at the 52nd Annual Meeting of the American Pancreatic Association, held in Miami Beach, Florida.
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