In conclusion, our results indicate that the innate and adaptive inflammatory immune response is an important pathogenetic mechanism of CeD and that IL27, IL21, IL2, IL1β, TNF, colony-stimulating factor 2 (CSF2) and IL7, as well as type I (IFNA1, IFNA2) and type II (IFNG) interferons, are the soluble factors orchestrating this inflammatory response. The gene discussed is IL21; the disease is cranioectodermal dysplasia.