In addition to shutting off translation to suppress viral replication, SGs serve as platforms for the RLR-mediated IFN response.8 Multiple PRRs and intermediate signaling molecules, including RIG-I, TRIM25, and PKR-activating protein (PACT), are present in avSGs during viral infection or nucleic acid transfection,16 and SG marker proteins are crucial for the RLR- and cGAS-STING-mediated IFN response.10 Since NSP5 and N proteins affect SG formation, we hypothesized that both proteins may negatively regulate the type I and type III IFN response. The gene discussed is STING1; the disease is viral infectious disease.