FCGR3A and Epstein-Barr virus infection: On the one hand, a nonessential role for NK cells was put forward because T−NK− patients with severe combined immunodeficiency (SCID) who recovered T but not innate lymphoid cells after HSCT were not susceptible to severe EBV infection over a long follow-up period [52]; a further argument is that patients with IEIs that affect NK cell development and/or function (i.e., mutated GATA2, MCM4, RTEL1, GINS1, IRF8, and FCGR3A) and predispose to severe/fatal herpesvirus infections [12] might have defects in other immunological compartments, at least in some cases [38,51].