[11] Osteoprotegerin (OPG) inhibits RANK:RANKL signaling by acting as a “decoy receptor” for RANKL, rendering it inaccessible for RANK binding and downstream signaling. [10] Mice deficient in OPG develop severe osteoporosis and prominent vascular calcification at an early age. [12] In hypercholesterolemic Ldlr−/− mice, exogenous OPG does not inhibit development of atherosclerosis, but prevents calcification of the aorta, [13] by mechanisms which have not been fully elucidated. Here, TNFRSF11B is linked to osteoporosis.