These findings are of major significance for understanding the pathophysiology of CeD, as they highlight the previously unappreciated importance of interleukin-2 together with interleukin-8 and interleukin-10 in driving the gluten-specific CD4+ T cell response responsible for the early immune events and clinical symptoms observed after gluten exposure (23). The gene discussed is IL10; the disease is cranioectodermal dysplasia.