In particular, potential CeD patients do not display an accumulation of IE-CTLs with an active killer phenotype (upregulated granzyme B expression, upregulated activating NK receptor expression, downregulated inhibitory NK receptor expression) and also lack upregulation of the pro-inflammatory cytokine IL-15 and the non-classical MHC class I stress molecules MICA/B and HLA-E in intestinal epithelial cells (25, 35, 36), immune features that are both required for the development of villous atrophy. The gene discussed is HLA-E; the disease is cranioectodermal dysplasia.