In the past, exogenous contaminants like 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and B(a)P were considered the only ligands of AHR, and TCDD-mediated sustained AHR activation often leads to toxic results such as cell cycle arrest, chloracne and increased atherosclerosis [2–5]. Here, AHR is linked to atherosclerosis.