Upon activation, RLRs and cGAS stimulate adaptor molecules MAVS and STING, respectively, to activate downstream signaling pathways that eventually trigger the expression of antiviral or immunoregulatory cytokines, such as interferons (IFNs).4 In addition to sensing viral components, the RLRs and cGAS pathways are reported to mediate sterile inflammation in the absence of infection induced by self-nucleic acids, such as in autoimmune disorders.5 Whether host nucleic acids can mediate antiviral immunity is poorly understood. This evidence concerns the gene STING1 and infection.