The striking similarities between clinical and biological features of SAVI syndromes and severe COVID-19, as well as other studies on the role of STING on T and B lymphocytes (Table 1), support the hypothesis of some delayed over-signaling downstream of cGAS-STING in severe COVID-19, despite initial inhibition of the STING-TBK1-IRF3 axis (and IFN secretion) by papain-like-proteases contained within the NSP3 and NSP16 proteins (98) (Figure 1). The gene discussed is IFNA1; the disease is COVID-19.