During the early stages of RNA viral infection, the exposure of viral genomic RNA in the cytoplasm of infected cells is known to trigger the activation of the RLR pathway.15–18 Accumulating evidence indicates that RNA viral infection can also lead to the activation of STING because of viral–cellular membrane fusion and viral infection-induced mitochondrial damage.19–21 Viral structural proteins and virion-associated accessory proteins of SARS-CoV-2 (Fig. 1a) are more likely to be involved in the suppression of host innate immune responses during the initial stages of viral infection. This evidence concerns the gene STING1 and viral infectious disease.