As expected, acetate lost the capacity to enhance IFN-I production and IRF3 phosphorylation in Mavs−/− BMDM (Fig. 5j, k), nor to protect against IAV infection in Mavs−/− mice (Fig. 5l), demonstrating that MAVS was indeed involved in the mechanism by which acetate protected the mice from viral infection. Here, MAVS is linked to viral infectious disease.