This is supported by a growing body of literature linking chronic DUOX2 and iNOS signaling to inflammatory bowel disease (IBD) and microbial dysbiosis.53,55,56 For example, both colonic DUOX2 and iNOS are upregulated during the early onset IBD57,58 while DUOX2 is highly responsive to a dysbiosis microbiome isolated from IBD patients.15 Future studies that delineate the role of stress-induced modifications to DUOX2 and iNOS activity may help unravel the complex etiology of stress-associated inflammatory bowel diseases. This evidence concerns the gene DUOX2 and inflammatory bowel disease.