So far, several theories have been proposed to define the mechanisms linking HLA-B*51 to BD and, similarly to the case of HLA-B*27 and AS, they reflect intrinsic properties of the molecule (i.e., being a “slow-folding” MHC molecule during peptide loading) and extrinsic features implying the presentation of self-peptides to autoreactive CD8+ T cells or NK cells [60,61]. The gene discussed is HLA-C; the disease is Behcet disease.