In conclusion, our data showed that TRPV2 overexpression was correlated with poor EFS, OS and bone lesions in MM patients and involved in osteoclastogenesis by activating Ca2+-calcineurin-NFATc3 signaling pathway, leading to the excessive secretion of inflammatory cytokines and RANKL, which in turn involved in the progression of osteoclastic differentiation. Here, TNFSF11 is linked to Miyoshi myopathy.