Briefly, with regard to the immunopathogenesis of CeD, a peculiar human leukocyte antigen (HLA) constellation favors gluten presentation by antigen-presenting cells (APCs) to CD4+ T helper (Th) cells, T cell–B cell interactions, and production of specific antibodies, resulting in immune-mediated killing of enterocytes and, macroscopically, in duodenal inflammation [3,4]. The gene discussed is CD4; the disease is cranioectodermal dysplasia.