Inhibitory pathways including the programmed cell death-1 (PD-1)/programmed death ligand-1 (PD-L1) interaction, cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) and killer cell immunoglobulin-like receptors (KIR) have also been shown to play important roles in MM immune dysfunction. This evidence concerns the gene CTLA4 and Miyoshi myopathy.