TNFRSF11B and endothelial dysfunction: Moreover, the demonstration that GM-CSF can significantly counteract the release of OPG, suggests that GM-CSF is able to interfere with the role of OPG in the vascular physiopathology, with significant clinical consequences since high circulating OPG levels are associated with endothelial dysfunction in several pathological conditions and represents a risk factor for cardiovascular disease progression [11, 34].