IFNλs have been increasingly implicated in antiviral therapies: 1) IFNλ administration in mice stimulated expression of Mx1 and protected IFNαR−/− mice from lethal influenza challenge [55]; 2) IL29 blocked HIV-1 replication by inhibiting virus integration and post-transcriptional events [56]; and 3) the combination of IL29 and IFNα or IL29 and IFNγ enhanced the induction of antiviral genes and effectively inhibited HCV and VSV replication [57]. The gene discussed is IFNA1; the disease is influenza.