KIR/HLA-C interactions can be altered by peptide loading and presentation by HLA-C [79, 80], which could suggest that interaction seen in GD and MS of the associated HLA-C molecules with a given autoantigen/s could be affecting KIR binding and that this interaction between KIRs and HLA-C could play a role in autoimmune onset [81, 82]. This evidence concerns the gene HLA-C and myeloid sarcoma.