Osteoclasts are stimulated by tumor‐produced cytokines that also stimulate receptor activator of NF‐κB ligand (RANKL) production by osteoblasts.7 We previously found that the IAP antagonist family of drugs activates NF‐κB in osteoclasts, enhances osteoclastogenesis, and promotes bone metastasis in male mouse models.8 We have also shown that tumor‐free male BALB/c and C57BL/6 mice receiving BV6, an IAP antagonist, over 4 weeks develop high turnover osteoporosis, dependent on the presence of NIK.8 Thus, IAP antagonists seem to provide a more favorable microenvironment for tumor growth in bone. This evidence concerns the gene TNFSF11 and neoplasm.