NFKB1 and peptic ulcer disease: Aside from CagA, which is the effector protein encoded at one end of cagPAI, probably the most virulent H. pylori factor and a true risk factor for peptic ulcer disease and gastric cancer, other bacterial cell wall components are also translocated via the T4SS, such as muropeptides or peptidoglycan, with the latter one being recognized by NOD1, which is an intracellular PAMP recognition receptor leading to the upregulation of proinflammatory immune responses via nuclear factor NF-κB activation [27].