In a mouse model of ovarian cancer cachexia, high circulating RANKL was sufficient to cause both accelerated bone loss and severe muscle atrophy; treatment with osteoclast-targeted therapies (denosumab or bisphosphonate zoledronic acid, which inhibit RANKL signaling) not only preserved bone mass but also significantly attenuated muscle wasting and weakness [106]. This evidence concerns the gene TNFSF11 and ovarian carcinoma.