It is well known that pancreatic inflammation accelerates the development andprogression of pancreatic cancer, which is, at least in part, mediated by ROS.DUOX2 seems to be involved in this process, once INF-γ increases its expressionand activity through the activation of the Jak-Stat1 and p38-MAPK pathway inhuman pancreatic cancer cell lines (Wuet al., 2011). This evidence concerns the gene STAT1 and pancreatic neoplasm.