In the primary X-linked immunodeficiency with magnesium defect, the Epstein-Barr virus infection, and neoplasia (XMEN), magnesium transporter 1 (MAGT1) is mutated and the diminished intracellular magnesium levels compromise glycosylation and surface expression of NKG2D [88]. This evidence concerns the gene KLRK1 and Epstein-Barr virus infection.