However, chronic cerulein-induced pancreatitis is initiated via a trypsinogen activation-independent inflammatory response, where cerulein stimulates acinar cells via the cholecystokinin receptor (G protein-coupled receptor) and the protein kinase C (PKC) pathway or the phosphatidylinositol 3-kinase (PI3K) pathway and the release of intracellular calcium, which in turn activates nuclear factor kappa B (NF-kB) [52]. The gene discussed is PRRT2; the disease is pancreatitis.