While several mechanisms have been postulated [28], a widely accepted hypothesis is that shorter telomeres lead to CHD through major SASP factors in different senescent cell types that contribute to atherosclerosis, e.g., IL-6 (forming atherosclerotic plagues and causing thrombosis), TNF (recruiting more immune cells and forming atherosclerotic plaques), and VEGF (promoting plaque angiogenesis and vascular remodeling) in senescent endothelial cells [29]. The gene discussed is IL6; the disease is coronary artery disorder.