Indeed, the authors, analyzing the mechanism underlying the protective status conferred by HLA-DRB1*01:01 and HLA-DRB1*11:01 alleles against multiple sclerosis, demonstrated the involvement of the HLA-DM-mediated lower efficiency to bind antigenic peptide to the antigen peptide groove of the protective allele with consequent failure of peptide presentation at the cell surface and possible alleviation of inflammatory/autoimmune processes39. The gene discussed is HLA-DMA; the disease is multiple sclerosis.