ERAP1 and ankylosing spondylitis: However, in HLA-B27-associated ankylosing spondylitis, the strong genetic interaction of ERAP1 with HLA-B*27 was independent from genetic associations with KIR genes, suggesting that the disease mechanisms of ERAP and HLA class I may be mostly distinct from interaction of KIRs with HLA class I (138), and perhaps represent complementary mechanisms such as shown for free heavy chain expression by HLA-B27 and KIR interaction (131), while ERAP may mediated antigen-specific T cell responses.