TRIM28 was demonstrated to inhibit the induction of type I IFNs by targeting IRF7 for SUMOylation after viral infections (16), suppress interleukin (IL)-6–induced STAT3-dependent gene expression by dephosphorylating STAT3 (17), or deacetylate NF-κB/p65 by disrupting the interactions among STAT3, p300, and NF-κB/p65, leading to reduced IL-6 production (18). This evidence concerns the gene NFKB1 and viral infectious disease.