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This commentary refers to the recent clinical study by Cohen et al., which investigated the efficacy of denosumab, a neutralizing antibody against receptor activator of nuclear-factor κB ligand (RANKL) in blocking structural joint damage in patients with rheumatoid arthritis. RANKL is an essential factor for the differentiation and activation of osteoclasts and for bone resorption. Therapeutic targeting of RANKL in patients with rheumatoid arthritis is, therefore, considered a promising tool for inhibiting the erosive joint damage that results from osteoclast-mediated bone resorption. A series of preclinical studies has suggested that RANKL has a key role in structural joint damage and can, therefore, be considered an interesting therapeutic target for blocking joint damage associated with arthritis. The study by Cohen et al. has highlighted these concepts by showing that blockade of RANKL with a neutralizing antibody halts structural deterioration of joints effectively in patients with rheumatoid arthritis.