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. Here, S100A8 is linked to infection.