In support of this hypothesis, we demonstrated that exposure of human colorectal cancer cells to clinically-achievable concentrations of the NOX (and related flavin dehydrogenase) inhibitors diphenylene iodonium [DPI] or 2-di-thienyl-iodonium [DTI], which decreased intracellular ROS levels, blocked IL-4- and IL-13-induced phosphorylation of STAT1, 3, and 6, as well as signaling through the mitogen activated protein kinase [MAPK] pathway. This evidence concerns the gene IL4 and colorectal cancer.