The fact that denosumab, which is approved for treatment of osteoporosis and skeletal-related events in cancer patients, restored platelet-mediated suppression of NK reactivity not only confirmed the specific involvement of RANKL; it also provides a potential explanation for recent clinical findings obtained upon application of denosumab for prevention of skeletal-related events in breast cancer patients, which suggest that denosumab treatment may influence disease-free survival [28]. The gene discussed is TNFSF11; the disease is cancer.