Likewise, NO can inhibit leucocyte adhesion to the vessel wall by either interfering with the ability of the leucocyte adhesion molecule CD11/CD18 to bind to the endothelial cell surface or by suppressing CD11/CD18 expression on leucocytes [12–15] resulting in atheroma formation which in turn contributes to the formation of a soft plaque which increases the risk of unstable angina, thrombosis, and acute myocardial infarction [16]. The gene discussed is ITGB2; the disease is angina pectoris.