Thus, whereas in vivo and in vitro IFNα treatment prompts BLyS upregulation20, 21, the therapy with an anti-IFNα monoclonal antibody reduces BLyS expression in SLE patients22, suggesting a cooperative action between BLyS and IFNα in the aetiology of SLE. Here, IFNA2 is linked to systemic lupus erythematosus.