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Physiological redox homeodynamics is maintained mainly by NRF2\/KEAP1, NF-\u03baB, protein tyrosine phosphatases, peroxisome proliferator-activated receptor-\u03b3 coactivator 1\u03b1 (PGC1\u03b1), and normal autophagy. Depletion of reduced glutathione (GSH) in the pancreas is a hallmark of acute pancreatitis and is initially accompanied by disulfide stress, which is characterized by protein cysteinylation without increased glutathione oxidation. A cross talk between oxidative stress, MAPKs, and NF-\u03baB amplifies the inflammatory cascade, with PP2A and PGC1\u03b1 as key redox regulatory nodes. In acute pancreatitis, nitration of cystathionine-\u03b2 synthase causes blockade of the transsulfuration pathway leading to increased homocysteine levels, whereas p53 triggers necroptosis in the pancreas through downregulation of sulfiredoxin, PGC1\u03b1, and peroxiredoxin 3. Chronic pancreatitis exhibits oxidative distress mediated by NADPH oxidase 1 and\/or CYP2E1, which promotes cell death, fibrosis, and inflammation. Oxidative stress cooperates with mutant KRAS to initiate and promote pancreatic adenocarcinoma. Mutant KRAS increases mitochondrial reactive oxygen species (ROS), which trigger acinar-to-ductal metaplasia and progression to pancreatic intraepithelial neoplasia (PanIN). ROS are maintained at a sufficient level to promote cell proliferation, while avoiding cell death or senescence through formation of NADPH and GSH and activation of NRF2, HIF-1\/2\u03b1, and CREB. Redox signaling also plays a fundamental role in differentiation, proliferation, and insulin secretion of \u03b2-cells. 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