This hypothesis exists at the confluence of established risk factors for coronary artery disease, including genetic susceptibility, polymorphisms predisposing to hypertension [126–128], diabetes [126] and hypercholesterolaemia and substantial new data implicating vascular inflammation [119, 129], endothelial dysfunction [119, 130], leptin dysregulation [104] and viral infection [131, 132] in the pathogenesis of vascular disease. This evidence concerns the gene LEP and viral infectious disease.