The observation that these genes are increased in SLE compared to IFNβ-treated MS might be explained by the indication that IFNβ, in contrast to IFNα, might more potently activate a broader range of signaling proteins, including ISGF3 and IRF8, resulting in relatively less activation of the GC-A genes by IFNβ. This evidence concerns the gene STAT2 and systemic lupus erythematosus.