Similarly, we demonstrated the expression of sclerostin by myeloma cells and the possibility that its contribution in the development of MM bone disease could be related to both a direct induction of OB suppression with reduced bone formation and an indirect activation of OC bone resorption through the unbalanced RANKL/OPG ratio [54–62]. The gene discussed is TNFRSF11B; the disease is Miyoshi myopathy.