TNFRSF11B and Miyoshi myopathy: Mesenchymal stem cells (MSCs), the progenitors of OBs, readily contribute to MM-BD by promoting OC formation and activity at various levels (increasing RANK-L to OPG expression, augmenting secretion of activin A and production of Wnt5a, etc.), thus further contributing to OB/OC uncoupling in MM osteolytic lesions [85].