Overall, MM cells increase OC formation through activation of the RANKL-NF-κB signaling pathway and suppress bone formation through factors in the TME, such as DKK1, sclerostin, MMPs, activin A, integrins and TGF-β, etc. MMP-13 is the main OCs inducer while activin A is increased in MM patients with bone lesions and the inhibition of OBs differentiation and mineralization [76]. The gene discussed is SOST; the disease is Miyoshi myopathy.