TRPV2 up-regulates intracellular calcineurin protein, promoting the dephosphorylation of NFATc3 and accelerating NFATc3 to enter the nucleus, thereby enhancing the synthesis and secretion of osteoclast-related factors (such as Receptor Activator of Nuclear Factor-κ B Ligand (RANKL)) in MM cells, ultimately leading to MBD [13]. Here, NFATC3 is linked to Miyoshi myopathy.