Despite this low incidence, both forms of chronic pancreatitis have provided substantial evidence for putative inflammatory mechanisms contributing to pancreatic cancer development and progression, including proinflammatory cytokines, nuclear factor-κB (NF-κB), cyclooxygenase-2 (COX-2), peroxisome proliferator-activated receptor-γ (PPARγ), nitric oxide (NO) synthesized by inducible NO synthase (iNOS), DNA damage caused by release of proteolytic enzymes and ROS, and somatic mutations in oncogenes (e.g., K-ras) and tumor suppressor genes (e.g., p53, p16, DPC4/Smad) [47-49]. This evidence concerns the gene PTGS2 and pancreatic neoplasm.