In conjunction with the drastic upregulation of the HLA-E on enterocytes in coeliac disease as compared to healthy individuals, these data suggest that selective upregulation of the CD94/NKG2C in place of inhibitory CD94/NKG2A may be a mechanism of tipping the balance toward effector function of T-IEL in disease (Table 2). The gene discussed is KLRC1; the disease is celiac disease.