Many studies have shown that IBD is correlated with an increased activity of T cells secreting IL-17 and IL-22 cytokines [118] and a decrease in that of Tregs [119], which leads to an imbalance in the T17/Tregs ratio that mediates an exaggerated immune response, intestinal injury, and, therefore, the development and maintenance of IBD. This evidence concerns the gene IL17A and inflammatory bowel disease.