IL-22, an important factor in the pathogenesis of UC as demonstrated by experiment models of colitis [5], induces the expression of tight-junction proteins (e.g., occludin and ZO-1) to facilitate gut epithelial resistance to colitis, indicating that IL-22 protects the intestinal mucosa from inflammation by upregulating the production of tight-junction proteins [6]. The gene discussed is OCLN; the disease is colitis.