Any difficulty differentiating HP from the nonhereditary form on the basis of biochemical and laboratory differences was mitigated by the discovery of a genetic difference: a 1996 study of five kindreds with hereditary pancreatitis revealed that an arginine-histamine substitution at residue 117 of the cationic trypsinogen gene, PRSS1, was associated with the phenotypic expression of acute pancreatitis due to failure of the affected trypsinogen, leading to autodigestion of the pancreas [35]. This evidence concerns the gene PRSS1 and hereditary chronic pancreatitis.