CCN3 in conditioned medium from prostate cancer cells favours osteoclastogenesis via both RANKL-dependent and RANKL-independent pathways in vitro and forced overexpression of CCN3 in PCa and LnCAP C4-2 cells enhances osteolytic potential and TRAP-staining in metastatic lesions (Chen et al. 2013b). The gene discussed is TNFSF11; the disease is prostate cancer.