Contrary to claudin-1, claudin-2-overexpressing mice exhibit higher resistance to experimental colitis by showing decreased cell apoptosis, increased epithelial proliferation and immune tolerance, brought about by downregulation of IL-6-induced NF-κB as well as STAT3 signaling and upregulation of Treg cell population as well as immunoregulatory cytokine TGF-β (93). The gene discussed is CLDN2; the disease is colitis.