S100A8 and angina pectoris: Since CagA stimulates the nuclear factor kappaB (NF-κB) signalling pathway in a cell-autonomous manner53, 54 hyperactivated NF-κB in CagA-delivered endothelial cells may promote atherosclerosis, a chronic inflammatory condition leading to endothelial cell dysfunction and eventually plaque formation and evolution, thereby predisposing individuals to coronary heart diseases, such as angina pectoris and myocardial infarction55.