Evidence supporting the theory of epitope spreading in DH include: (i) the high sequence homology between tTG and eTG (9); (ii) the presence of an autoimmunity also against neuronal TG (or TG6), which is also highly similar to tTG and eTG, in both CD and DH (99); (iii) the lower prevalence of anti-eTG IgA autoantibodies in pediatric compared to adult CD patients, which (iv) parallels the decreased, albeit not abolished, incidence of DH during childhood (23, 104). The gene discussed is CD79A; the disease is Autoimmunity.