Notably, these authors described the molecular pathways that have to be modulated for counteracting the detrimental effects of osteoporosis pathology, focusing on the role of β-catenin in osteoblast proliferation and bone formation and of RANKL in bone resorption, but the molecular markers (like RUNX2, OCN, ALP, COL1α1, and OPN) that lead to the differentiation of human BM-MSCs in osteoblasts should also be considered. The gene discussed is RUNX2; the disease is osteoporosis.