Previous research on extracellular pathogens, such as Yersinia pseudotuberculosis, enteropathogenic Escherichia coli (EPEC), and enterohemorrhagic Escherichia coli (EHEC), demonstrated that bacterial effectors like YopJ and NleE acetylate and antagonize TAK1, IKKα/β, and MAPK kinases (MAPKKs), thereby limiting NF-κB and MAPK-driven pro-inflammatory cytokine expression and promoting RIPK1-dependent caspase-8 activation, which is crucial for controlling bacterial infection and dissemination in vivo (27, 28). This evidence concerns the gene NFKB1 and bacterial infectious disease.