Specifically, upon herpes simplex virus type I (HSV-1) and HCMV infections, IFI16 interacts with cGAS through the PYRIN domain [71], but whereas IFI16 promotes an antiviral response through IFN-β induction, cGAS preferentially activates the stimulator of interferon genes (STING)/ TANK-binding kinase 1 (TBK-1)/ interferon regulatory factor 3 (IRF3) pathway to induce cell death [69,71]. This evidence concerns the gene IRF3 and cytomegalovirus infection.