In response to infection, CD4+ T cell-specific Stat3−/− mice have increased HSV-1-specific CD8+ T cells that express lower levels of KLRG-1 and IFNγ, suggesting that antiviral CD8+ T cell function relies in part on their cooperation with STAT3-competent CD4+ cells (Yu et al. 2013). The gene discussed is CD4; the disease is infection.