The development of immunotherapeutic modalities for MM has been delayed because of immune evasion by tumor cells through decreased expression of tumor-specific antigens, enhanced expression of inhibitory ligands such as programmed cell death ligand 1 (PD-L1) or major histocompatibility complex (MHC) molecules, and the recruitment of regulatory T cells (Tregs) or myeloid-derived suppressor cells (MDSCs), both of which work as immune suppressive cells [20,21,22,70,71,72,73,74]. Here, HLA-C is linked to neoplasm.