According to previous studies, CCL5 should also be expressed in malignant cells to promote the secretion of CXCL9 by immune cells through epigenetic regulation, thus jointly recruiting T cells, whose infiltration and activation exert immune killing effects to inhibit tumor progression [65]; ligand-receptor interaction between CCL5 and CCR1 is notably active in the monocyte-plasma communication in MM patients with stage III [66]. This evidence concerns the gene CCR1 and Miyoshi myopathy.