Actually, H. pylori-induced interaction between TAK1 and IKK complex may be involved in NF-κB initial activation in a T4SS-dependent manner during early infection, while CagA may be play a role in extend the activation of NF-κB during persistent infection because CagA takes more time to be delivered into the host cells and regulates its target proteins or signaling pathways. This evidence concerns the gene NFKB1 and infection.