UCP2 downregulation associates with increased oxidative stress, atherosclerosis, vascular damage and shorter lifespan in mice.9, 10, 11, 12 UCP2 overexpression significantly prevented ROS production in endothelial cells and preserved endothelial function by reducing ROS levels.13, 14 Consistently with its ability to decrease endogenous mitochondrial ROS production and to maintain normal mitochondrial membrane potential and ATP levels, a neuroprotective effect of UCP2 has been previously described both in vitro and in vivo. This evidence concerns the gene UCP2 and atherosclerosis.