Overall, the current observations propose two major mechanisms by which CCL3 and/or CCL5 released by tumor cells and their receptors support MM progression: the first is the ability to disrupt bone homeostasis and induce bone destruction, and the second is the bone marrow homing of MM cells [35] due to the expression of CCR5 and CCR1. The gene discussed is CCL5; the disease is Miyoshi myopathy.