The results showed that F2RL1 (PAR-2) and phosphorylated protein kinase C α (PRKCA), upstream effectors of the JAK1, STAT5, and JAK1/STAT5 canonical pathways, were significantly upregulated in pancreatic cancer cells with the PRSS1_R116C mutation vs OE or LV-NC counterparts; the same expression pattern was applied to REAL (a molecule in the non-canonical JAK1/STAT5 pathway). The gene discussed is PRKCA; the disease is pancreatic neoplasm.