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. This evidence concerns the gene NFKB1 and coronary artery disorder.