Serum anti‐TG2‐IgA antibody tests are widely employed for diagnosis of CeD due to their excellent sensitivity and specificity.[9] Moreover, IgA and IgM plasma cells specific for TG2 are abundant as effector B cells in the small intestine lamina propria of CeD patients.[10] To explain the connection between gluten exposure and the formation of TG2‐specific auto‐antibodies in CeD, it has been proposed that TG2‐specific B cells take up TG2‐gluten enzyme–substrate complexes via their B‐cell receptor (BCR), thereby allowing presentation of deamidated peptides to gluten‐specific CD4+ T cells. This evidence concerns the gene CD79A and cranioectodermal dysplasia.