Collectively, these results indicate that the different responses to infection in MAVS−/− and IRF3−/−IRF7−/− compared to IFNAR1−/−IL-28Rα−/− cells can not be ascribed to a lack of priming in the latter, but are most likely due to a residual production of IFN in MAVS−/− and IRF3−/−IRF7−/− cells, that, in the context of infection, is sufficient to ensure ISG induction. The gene discussed is IFNA1; the disease is infection.