The upregulation of HERVs, TRIM28, and SETDB1 and their positive correlations are suggestive clues of their contribution to the pathophysiology of CeD and might justify the persistent risk of developing, despite GFD, autoimmune diseases, neuropsychiatric disturbances, and cancers, all disorders characterized by enhanced HERV expressions and epigenetic alterations. This evidence concerns the gene SETDB1 and cranioectodermal dysplasia.