Given the evidence for the importance of IL-6, RORγt, total STAT3 and its activated form p-STAT3, and Foxp3 levels in the immunoregulation of the Th17/Treg axis and their correlation with the severity of both experimental colitis and human IBD [6,23,24,25,26], it can be assumed that these factors may be potential targets in the pharmacotherapy of IBD and normalization of their levels may lead to prevention or at least alleviation the symptoms of intestinal inflammation. The gene discussed is FOXP3; the disease is inflammatory response.