As mentioned, IFNAR-deficient lupus-prone mice were known to be protected from disease development and recently it was shown that lupus-prone 564Igi and NZBWF1 mice treated with an anti-IFNAR antibody resulted in a significantly reduced IFN signature and reduced lupus-associated CNS pathogenesis [29]. This evidence concerns the gene IFNA1 and systemic lupus erythematosus.