If endothelial cells are subjected to stressful conditions, such as hemodynamic stress, they over-express HSP60, which is then also presented on the cells’ surface, and the cross-reactive anti-HSP60 antibodies may damage the endothelial cells, thereby initiating a repair response which triggers endothelial dysfunction and the subsequent development of atherosclerosis (Figure 2) [87]. This evidence concerns the gene HSPD1 and endothelial dysfunction.