In the last decade, extensive research stemming from the observation of RANK-expressing RANKL-sensitive cancer cell lines from different tumor types, including BC [110–113], clearly corroborated that the RANKL-RANK pathway is a major mediator of breast physiology and carcinogenesis [107, 114–116] as recently reviewed by our study group [117]. This evidence concerns the gene TNFRSF11A and neoplasm.