TRPV2 and Miyoshi myopathy: In fact, in MM cells, switching from low to high Ca2+ conditions activated TRPV2 and induced osteoclastogenesis via the Ca2+-calcineurin-NFATc3 signaling pathway, ultimately leading to excessive secretion of inflammatory cytokines and nuclear factor kappa β (NF-κβ) ligand (RANKL), which contributed to the progression of osteoclastic differentiation (formation of osteoclasts).