All CeD patients have in their intestine proinflammatory CD4+ T cells that recognize posttranslationally modified gluten peptides in context of the disease associated MHC class II molecules HLA‐DQ2.5, DQ8, or DQ2.2.[1, 2] Even on a gluten‐free diet, low numbers of gluten specific CD4+ T‐cells remain in the memory T‐cell compartment.[3] These cells are rapidly reactivated when CeD patients eat gluten again.[3, 4] CeD is therefore a life‐long condition that requires strict dietary measures. The gene discussed is TOR1A; the disease is cranioectodermal dysplasia.