Following incubation with Cd, the Thr-391 variant was found to have lower intracellular Cd levels with accompanying less Cd-induced toxicity, decreased phosphorylation of mitogen-activated protein kinase-1 (MAPK1), and lowered NFκB activation; not surprisingly, the same differences were seen in vascular endothelial cells [68]; although the authors suggest that the ZIP8 Thr-391 variant is “therefore mechanistically responsible for lower serum HDL-Chol levels, coronary artery disease, and hypotension”—this connection remains to be elucidated in their study. The gene discussed is SLC39A8; the disease is coronary artery disorder.