ICAM1 and triple-A syndrome: ICAM1 and endothelial cells recruit circulating ITGB2, also known as CD18, and immune cells contribute to atherosclerosis; therefore, inhibition of ITGB2 can alleviate or even prevent the development of atherosclerosis.[26] Animal experiments have shown that treatment of mice with AAA using an anti-CD18 monoclonal antibody alleviates AAA expansion and reduces the inflammatory response,[27] indicative of the potential benefit of ITGB2 downregulation in patients with AAA.