Accordingly, RANKL/RANK signaling might promote dedifferentiation processes that induce EMT and “stemness” in normal breast epithelial and breast cancer cells [38], supporting the notion that RANKL/RANK-driven tumor initiation, progression, and metastasis relies on its ability to regulate self-renewal and activity of CSC-like cells with tumor- and metastasis-initiating capacity [38–41]. This evidence concerns the gene TNFRSF11A and neoplasm.