Because previous studies have documented the ability of NOX1-dependent ROS to produce genetic instability in mammalian cells [71], it is reasonable to suggest that the IL-4- or IL-13-mediated upregulation of NOX1 could play a role in the development of the colorectal cancers that occur in patients with inflammatory bowel disease or stimulate the progression of established colonic neoplasms. This evidence concerns the gene IL13 and colorectal cancer.