SPINK1 and pancreatitis: Recent years saw a surge in the development of genetically engineered mouse models where increased activation of mutant trypsinogens drive pancreatitis onset and progression.22, 23, 24, 25, 26, 27, 28 The availability of these models offers a fresh approach to address the role of heterozygous Spink1 deficiency in trypsin-mediated CP.