While it is possible that the later surge of MAVS-independent IFN-β induction is due to the activation of the cGAS-STING pathway by the release of mitochondrial and/or nuclear DNA upon YFV-induced cellular stress and structural damages in the later phase of the infection [13, 54, 55], the pathobiological significance of this MAVS-independent cytokine response deserves further investigation in infected animals. This evidence concerns the gene STING1 and infection.