It is known that treatment with denosumab, an anti-RANKL antibody, reduces the mammosphere-forming ability in BRCA1-mutated epithelial cells, in triple negative and in HER2-overexpressing breast-cancer cells, supporting the notion that tumor and cancer initiating cells have hyperactive RANKL signalling in primary and metastatic sites such as bone. This evidence concerns the gene TNFSF11 and neoplasm.