The pharmacological blockade of PPAR-γ signaling in CD may, however, be problematic, because PPAR-γ is essential for the maintenance of epithelial expression of a beta-defensin DEFB1 that protects against mucosal adherence of certain microorganisms, and its expression was found to be reduced in colonic CD [140]. The gene discussed is DEFB1; the disease is Cowden disease.