CD8A and Behcet disease: Despite several studies aimed at a deeper understanding of the BD basis, the contribution of HLA-B*51 and ERAP1 to the disease risk could be consistent with the involvement of a dysregulated CD8+ T response or with an aberrant NK cell activation likely caused by altered interactions with inhibitory leucocyte immunoglobulin-like receptors (LILRs) or killer immunoglobulin-like receptors (KIRs) [65].