This could be perceived either by KIR-ligand mismatching based on genotypes in an allogeneic transplantation setting, the use of clinically available monoclonal antibodies to block KIR (e.g., lirilumumab) or NKG2A (e.g., monalizumab) (41, 42), or by agents such as the proteasome inhibitors lactacystin, bortezomib and carfilzomib that have been shown to reduce HLA class I expression in MM (43–45). Here, KIR3DL1 is linked to Miyoshi myopathy.