Notably, UL31-mediated inhibition of cGAS appears to have a broad immune footprint, affecting multiple immune signaling archetypes, as infection with a UL31-deficient HCMV mutant strongly induced both ISG’s and NFκB target genes, and plasmid overexpression of UL31 in fibroblasts inhibited the activation of both ISRE-containing and NFκB reporter elements [81]. The gene discussed is NFKB1; the disease is infection.