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RANKing c-Jun in osteoclast development.

Pathological bone loss always reflects enhanced net osteoclastic activity. Rec-ognition and binding of the receptor activator of NF-κB (RANK) by RANK ligand (RANKL) is the key osteoclastogenic event, and the signaling cascades induced by this reaction therefore contain potential anti-osteoporosis thera-peutic targets. A study reported in this issue of the JCI documents that a piv-otal component of RANKL/RANK-mediated osteoclast recruitment involves sequential induction of the transcription factors c-Jun and nuclear factor of activated T cells 2 (see the related article beginning on page 475).