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Chronic pancreatitis is a fibroinflammatory dis-order characterized by irreversible pancreatic destruction leading to both exocrine and endo-crine organ failure. The hallmark of chronic pancreatitis is repeated cyclical fibroinflamma-tory responses to a primary insult such as alco-holic injury (Braganza et al., 2011). Intrapancreatic inflammation requires the activation of tran-scription factors, including NF-B and AP-1 which can be induced by the RANK ligand and TNF (Vaquero et al., 2001). However, the precise cellular and biochemical mediators in chronic pancreatitis are uncertain. An even more interesting feature of fibro-inflammatory pancreatic disease is the observation that chronic pancreatitis is the leading risk factor for the development of pancreatic cancer. Epi-demiological studies suggest that the incidence of pancreatic carcinoma in individuals suffering from chronic pancreatitis ranges between 1.4 and 2.7 % (Ammann et al., 1984; Lankisch et al., 1993). Overall, individuals with chronic pan-creatitis have a 16-fold greater lifetime risk of developing pancreatic adenocarcinoma than the general population (Jura et al., 2005). As such, the transition of chronic pancreatitis to pancreatic carcinoma represents an exemplary clinical example of the paradigm of chronic inflamma-tion degenerating into neoplasia. Although the cellular and biochemical links between benign and malignant pancreatic disease remain poorly understood, a distinct feature of pancreatic can-cer, and a commonality with chronic pancreatitis, is the extensive fibroinflammatory stroma sur-rounding the transformed ductal epithelial cells (Ricci et al., 2005). This suggests that th