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]. The gene discussed is TNFRSF11B; the disease is cardiovascular disorder.