CCL2 was previously shown to be in vitro and in vivo essential for the growth of MM [51, 52], and 15a miR was reported to inhibit the proliferation and induces apoptosis in MM cells through targeting AKT serine/threonine-protein-kinase (AKT3), ribosomal-protein-S6, MAP-kinases, and NF-κB-activator MAP3KIP3 [53]. This evidence concerns the gene AKT1 and Miyoshi myopathy.