Arising from the interplay of genetic, environmental, and immunologic factors, CeD pathogenesis involves a complex cytokine network induced by gluten intake, including INF-γ produced by TH1 cells, IL-15, INF-α, and possibly IL-1834 and IL-21,41 whereas an increase in gut intraepithelial γδ T cells is considered a hallmark of CeD and their role in the diagnostic approach seems promising.42 The gene discussed is IL15; the disease is cranioectodermal dysplasia.