RANKL favors the expansion of the local Treg population in bone metastatic prostate cancer (96), promotes M2–macrophages polarization in breast cancer models of lung metastasis (97, 98), interferes with NK anticancer activity in acute myeloid leukemia (51), is necessary for T cell tolerance in a melanoma model (99), where successful results were obtained by a combinatory treatment of RANK/RANKL blockade with anti-CTLA-4 (100). This evidence concerns the gene TNFSF11 and breast cancer.