Recent studies have evidenced that gluten components, such as gliadin and other prolamins, can bind the C-X-C motif chemokine receptor 3 (CXCR3), which can induce the increase of intestinal zonulin and disassemble intercellular tight junctions of the intestinal mucosa, thus altering gut paracellular permeability and substantially contributing to the pathogenesis of CeD [11,12,13]. This evidence concerns the gene CXCR3 and cranioectodermal dysplasia.