Our results showed that STING (S366D) mutant enhanced the interaction between STING and OTULIN, while weakening the interaction between STING and HOIP (Figure S6L, Supporting Information), indicating that the phosphorylation of STING (S366) site functions as a switch to regulate the interactions between STING and HOIP or OTULIN at the different stages of viral infection. This evidence concerns the gene OTULIN and viral infectious disease.