In contrast to 5-ASA agents, DKT appears to work by upregulating endogenous epithelial ADM, which has been shown in mouse and rat models of CD to attenuate mucosal damage and inflammatory adhesions, suppress mucosal proinflammatory cytokine (TNF-α and IFN-γ) release and improve the blood flow in ischemic segments [15, 26]. The gene discussed is TNF; the disease is Cowden disease.