To address whether OPG acts as a mediator or inhibitor of calcification, Morony and colleagues used recombinant OPG (Fc-OPG) to treat a mouse model of atherosclerosis and found that treatment reduces the calcified lesion area, supporting the role of OPG as an inhibitor rather than a mediator of calcification [96]. This evidence concerns the gene TNFRSF11B and atherosclerosis.