In fact, recent in vivo experimental data has demonstrated that at the bone level in human osteoporosis fracture there is an increase of osteoblasts inhibitors, such as the Wnt protein family molecules DKK-1 and sclerostin (SOST), and of osteoclastogenesis activators, such as RANKL, M-CSF and TGF-beta; moreover, this study demonstrated that an increase of RANKL/OPG ratio is present, further confirming the association of the RANK/RANKL/OPG axis in the pathogenesis of bone disruption in osteoporosis fractures [22]. Here, TNFRSF11A is linked to osteoporosis.