Based on these findings, we proposed that the effect of the PRSS1_R116C mutation could be mediated as follows: PRSS1_R116C mutation promoted pancreatic carcinogenesis and tumor development via the canonical JAK1-STAT5 pathway, which was triggered by upregulation if trypsin, which activated its cell surface receptor PAR-2 (F2RL1). Here, JAK1 is linked to neoplasm.