It has also been demonstrated that the interaction between Pb exposure and CHD risk is modified by polymorphisms of the vitamin D receptor (VDR), heme oxygenase-1 (HMOX1), apolipoprotein E (APOE), angiotensinogen (AGT), and glutathione S-transferase (GSTP1) genes, indicating potential underlying mechanisms [24]. The gene discussed is HPGDS; the disease is coronary artery disorder.