Epstein–Barr virus (EBV) infection in humanized mice can recapitulate both the lytic and latent phases of infection, stimulate EBV‐induced lymphomas,68 create specific CD8+ T‐cell response and expansion,69, 70 NK‐cell‐mediated EBV restriction, activation and plasmacytoid dendritic cell depletion71, 72 and both latent and lytic EBV antigens can be detected.73 Tumorigenesis from EBV infection can develop in both the peripheral blood injection model (e.g. huPBLscid) and in the CD34+ HSC injection models upon depletion of human cell subsets controlling oncogenesis.5, 27. The gene discussed is CD8A; the disease is infection.