AhR activation with polycyclic aromatic hydrocarbon and a prototypical AhR agonist, benzo[a]pyrene resulted in an induction of Cyp1a1, which rapidly metabolized estrogen receptor ligand, 17β-estradiol and inhibited the protective effects of estrogen signaling, leading to the NAFLD pathology including hepatic steatosis characterized by triglyceride accumulation and hepatotoxicity in a high-fat diet model [87,88]. The gene discussed is AHR; the disease is fatty liver disease.