The mechanism of response to HSV appears to depend on the infectious viral dose: At a high viral dose (multiplicity of infection -MOI of 15), infected hiPSC-derived microglia induced cGAS-dependent apoptosis, which consequently downmodulates local immune response, whereas at a lower viral dose (MOI of 5), cGAS activation induced Type I IFN production and antiviral activity [241]. This evidence concerns the gene CGAS and infection.