In this context, we focused on targeted analysis based on the state-of-art knowledge of BPs mechanism of action in osteoblasts, and evaluating the role of RANK/RANKL and purinergic pathways, known for their importance both in CLL progression and osteoporosis [33–40], we demonstrated that the BPs effects observed do not operate through these conventional pathways. The gene discussed is TNFRSF11A; the disease is osteoporosis.