However, when stressed by classical atherogenic risk factors, such as high blood pressure, obesity, diabetes, and cigarette smoking, HSP60 is expressed in the mitochondria and then transported to the cytoplasm and finally to the surface of endothelial cells at the predisposed atherosclerotic sites and thus acts as a “danger signal” for pre-existing HSP60 reactive T cells. Here, HSPD1 is linked to diabetes mellitus.