Acetate or propionate treatment alone did not induce detectable IFN-I responses prior to infection in BMDMs (Fig. 3b and Supplementary Fig. S4D), suggesting that endogenous microbiota-derived SCFA signaling through GPR43 is not sufficient to activate MAVS, but requires a second signal during viral infection to fully activate IFN-I pathways. The gene discussed is MAVS; the disease is viral infectious disease.