At present, a valid hypothesis is that the immune pathogenesis of DH starts from hidden CD in the gut with a TG2, and possibly also a TG3, autoantibody response and evolves into an immune complex deposition of high avidity IgA TG3 antibodies together with the TG3 enzyme in the papillary dermis. This evidence concerns the gene CD79A and dermatitis herpetiformis, familial.