As IFNγ has been shown to regulate MHV68 reactivation from macrophages in the peritoneum, but not reactivation from splenic B cells [6], we would predict that the Vβ4+ CD8+ T cells traffic to sites in which infection is less tightly controlled, to suppress MHV68 reactivation through the secretion of IFNγ in a paracrine fashion. The gene discussed is IFNG; the disease is infection.