Interestingly, molecular studies on IEI due to mutations in MAGT1 (referred to as ‘X-linked MAGT1 deficiency with increased susceptibility to EBV-infection and N-linked glycosylation defect’, XMEN), CD70, and CARMIL2 have demonstrated that these three distinct diseases share a common reduction of the activating NKG2D receptor and, hence, of the cytotoxic activity of CD8 T and NK cells [46,47,48]. This evidence concerns the gene MAGT1 and Epstein-Barr virus infection.