This leads to robust activation of gsTcells that subsequently stimulate B cells to start producing auto antibodies to TG2 and deamidated gluten peptides1,2 and activate CD8+ intraepithelial lymphocytes (IELs) to attack intestinal epithelial cells, leading to the villous atrophy that is characteristic of CeD. This evidence concerns the gene TGM2 and cranioectodermal dysplasia.