The chemokine CXCL12, while being able to direct homing of MM cells to the BM, has also been shown to exhibit proliferation-inducing effects on MM cells.[7] The intercommunication between MM cells, SCs, osteoclasts, and osteoblasts through factors such as receptor activator of nuclear factor-κB ligand, macrophage inflammatory protein-1α, dickkopf-1, monocyte chemotactic protein-1 (MCP-1), and interleukin 3 (IL-3) have been demonstrated to influence bone resorption by osteoclasts and bone formation by osteoblasts thus leading to osteolytic bone lesions often seen in this disease. This evidence concerns the gene CCL2 and Miyoshi myopathy.