In support of the latter possibility, activated T cells have been shown to be refractive to TGFβ signaling in CD patients, due to enhanced expression of the TGFβ signaling inhibitor Smad7,26 with knockdown of Smad7 causing remission in some patients.3 In such a scenario, enhanced integrin αvβ8 expression by DC would result in increased TGFβ activation, but without causing a protective response in TGFβ-refractory colitic T cells. This evidence concerns the gene SMAD7 and Cowden disease.