Patients with osteoporosis exhibit increased osteoclast differentiation and activity, partly due to reduced suppression of receptor activator of nuclear κβ ligand (RANKL).8–10 Accordingly, the suppression of osteoclast activity is the main target for commonly used osteoporosis treatments, such as bisphosphonates or denosumab.11 Although current osteoporosis treatments decrease fracture risk, clinical management is limited by contraindications, adverse effects, and skeletal complications associated with long-term treatment with antiresorptive compounds, even after withdrawal.12–15. Here, TNFSF11 is linked to osteoporosis.