While rapid induction of type I interferons (IFNs) limits virus propagation, sustained induction of type I IFNs in the late phase of SARS-CoV-2 infection is associated with aggressive inflammation and poor clinical outcomes.2,30–40 The cGAS-stimulator of IFN genes (STING) pathway is upregulated in severe COVID-19, driving type I IFN immunopathology.30 Phosphorylation of STING was increased in the lungs of aged SIRT2 KO mice upon viral infection (Figures 1E and 1F), consistent with a role of SIRT2 in suppressing cGAS activation. Here, STING1 is linked to viral infectious disease.