The enhanced vulnerability of EBV-infected B cells upon HIV-1 coinfection may explain why these coinfected cells were preferentially observed upon CD8 depletion in vivo, and point toward HIV-1 superinfected EBV-transformed B cells being efficiently controlled by CD8+ T cells, even if their activity to protect from EBV-induced lymphomas is compromised by loss of CD4+ T-cell help due to HIV-1 infection. The gene discussed is CD4; the disease is HIV-1 infection.