While overexpression of human apoA-II in mice increased atherosclerosis susceptibility [52] and converted HDL to proinflammatory particles with a diminished antioxidant capacity [23,24], overexpression of human apoA-II in rabbits reduced aortic and coronary atherosclerosis, accompanied by an increased cholesterol efflux and antioxidant activities of HDL [53]. Here, APOA2 is linked to atherosclerosis.