The great majority of untreated CeD patients are seropositive for gluten-dependent antibodies against gluten-derived gliadin peptides and autoantibodies against TG2 (anti-TG2 and endomysial antibodies), another member of the TG family of enzymes and the main autoantigen in CeD (7). The gene discussed is TGM2; the disease is cranioectodermal dysplasia.