Two sources have been proposed to increase HMGB-1 circulating levels, the local HMGB-1 release promoted by damaged immune cells such as monocytes, macrophages, endothelial cells cytokine-triggered, or the secretion from vascular smooth muscle cells (VSMCs) in atherosclerotic lesions [5, 37]. This evidence concerns the gene HMGB1 and Atherosclerotic lesion.