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. This evidence concerns the gene TRPV2 and Miyoshi myopathy.