Moreover, polymorphisms of the genes responsible for iAs biotransformation (e.g. arsenic-3-methyltransferase, AS3MT), oxidative stress (e.g. nitric oxide synthase 3, NOS3 and superoxide dismutase 2, SOD2), inflammation/endothelial dysfunction (e.g. intercellular adhesion molecule-1, ICAM1 and soluble vascular adhesion molecule­1, VCAM1); and inflammation (e.g. apolipoprotein E, APOE), can be attributed as one of the reasons for the difference in individual susceptibility to iAs-induced CVD11, 13, 15–18. This evidence concerns the gene APOE and endothelial dysfunction.