Decreased levels of OPG can lead to excessive activation of RANKL, resulting in an increase in the number of osteoclasts and bone resorption, which contributes to the development of osteoporosis.[175] OPG exerts its effects by binding to RANKL, thereby regulating bone remodeling and maintaining balance.[176] The role of OPG in the CNS is complex. The gene discussed is TNFRSF11B; the disease is osteoporosis.