In many cases of MM, the normal balance between bone resorption and new bone formation is disrupted, resulting in bone deterioration and the development of osteolytic lesions.159 Osteoclast activation-induced bone damage generally occurs around MM plasma cells rather than in normal BM.160 Furthermore, PCs obtained from osteolytic lesions exhibited upregulation of genes associated with myeloma-related bone disease, including DKK1, HGF, and TIMP-1, as well as recurrent downregulation of JUN/FOS, DUSP1, and HBB.122. This evidence concerns the gene TIMP1 and Miyoshi myopathy.