As speculated, anti-OPG administration partially reversed the beneficial effects of IL-37 on plaque area and vulnerability, increased ALP and BMP-2 levels but failed to alter participating cytokine titers (i.e., IL-10, IL-18 and TNF-α), suggesting the involvement of yet another mechanism (independent of OPG) via which IL-37 mediates atherosclerosis and CAC amelioration [105]. Here, TNFRSF11B is linked to atherosclerosis.