Apparently, downregulation of NKG2D is due to different causes, with the receptor being either destabilized by the loss of MAGT1-dependent glycosylation (in part also affecting CD70) [46] or, presumably, poorly expressed when co-stimuli are missing (i.e., CD70 and CARMIL2-mediated CD28 co-stimulation); notably, rescue of NKG2D expression and NKG2D-mediated cytotoxicity against EBV+ cell targets could be obtained by exposing MAGT1-deficient NK and CD8 T cells to Mg2+ in vitro [46], although Mg2+ supplementation in XMEN patients was not effective in a small study recently reported [49]. The gene discussed is CD8A; the disease is X-linked immunodeficiency with magnesium defect, Epstein-Barr virus infection and neoplasia.