Figure 1.

Two hit model for the pathogenesis of TCP. First hit contributing to the pathogenesis of TCP is likely to be loss of balance between activation events and degradation of active trypsin leading to presence of persistent “super-trypsin” within the acinar cell, which could occur due to mutations in one or more genes like SPINK1, CTSB, CTRC, other yet unidentified genes, resulting in inflammation. Presence of additional genetic and/or environmental factors, which constitute the second hit, may lead to one or more phenotypes such as stone formation, fibrosis, and/or diabetes mellitus. ¹Mutation in genes.