Finally, in an above-mentioned preclinical study, miR-155 overexpression could suppress CD47 on MM cells and re-sensitize drug resistant MM cell lines to bortezomib, further confirming the inhibition of CD47-SIRPα signaling could represent a promising treatment strategy to counteract the immunosuppressive TME of MM within the BM [149]. This evidence concerns the gene CD47 and Miyoshi myopathy.