In summary, the observation that the celiac autoantigen TG2 specifically catalyzes self-multimerization in a manner that preserves the dominant celiac anti-TG2 IgA epitopes is compelling as it may explain not only the low mutation rate and short lifetime of TG2 specific plasma cells, but also how, and why, the threshold for activation of self-reactive B cells can be reached in celiac disease. This evidence concerns the gene CD79A and celiac disease.