STING1 and viral infectious disease: Modification at this residue appears to impair the ability of pp71 to target the cGAS-STING-TBK1 pathway as a pp71 mutant that cannot be S-nitrosylated at this site more potently suppresses STING-mediated innate immune responses in the context of both ectopic expression and productive viral infection (Nukui et al., 2020).