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. The gene discussed is IL4; the disease is inflammatory bowel disease.