While causality remains unproven, collective data suggest that ERRγ may amplify RANKL/NF-κB signaling in the bone microenvironment, a hypothesis partially supported by studies in non-MM contexts showing ERRγ inhibition suppresses RANKL-mediated osteoclastogenesis [10] and parallels its role in NF-κB-driven bone remodeling in osteoarthritis [42]. This evidence concerns the gene TNFSF11 and Miyoshi myopathy.