Indeed, studies on tonsillar NK cells, which are mainly CD56bright as opposed to circulating blood NK cells, demonstrated that a subset of CD56bright NK cells with an immature phenotype (NKG2A+CD94+CD54+CD62L−) accumulated in the tonsils of EBV+ individuals and, once activated and tested by in vitro assays, displayed a superior capacity to release IFN-γ and restricted more efficiently both EBV infection and tumorigenic transformation of B cells if compared to other tonsil-derived or blood NK cell subsets [64,65,66]. The gene discussed is KLRC1; the disease is Epstein-Barr virus infection.