p31–49 induced IL-15 expression by LP dendritic cells and macrophages of CeD patients (21), and the p31-mediated upregulation of MICA could be blocked by α-IL-15 neutralizing antibodies (20), suggesting that this might be a mechanism of how the sensing of gluten and IL-15 is integrated to result in the expression of NKG2D and MICA and contribute to CeD pathogenesis. Here, KLRK1 is linked to cranioectodermal dysplasia.