It can induce a type I IFN response in a STING-dependent manner, trigger the NF-κB pathway by activating ERAdP or inhibiting RECON, induce an NLRP3-dependent inflammasome response, and activate host cell autophagy, promoting the production and secretion of signaling mediators such as cytokines, thus modulating the host defense against infection. This evidence concerns the gene NFKB1 and infection.