In 2010, Cagliani et al. studied the ERAPs susceptibility to HIV-1 infection and found that the polymorphisms in ERAP1 and ERAP2 genes may have been maintained through long-standing balancing selection, and that ERAP2 conferred resistance to an HIV infection likely via the presentation of a distinctive peptide repertoire to CD8+ T cells (Cagliani et al., 2010). The gene discussed is CD8A; the disease is HIV infectious disease.