The importance of type I IFN in the development of LN stems from experimental and clinical studies that show reduced autoimmunity in type I IFN receptor-deficient lupus-prone mice44, exacerbation of disease following administration of adenovirus encoding IFN-α to lupus-prone mice9,45, and the production of lupus-related antibodies in a significant percentage of patients whose hepatitis C was treated with IFN-α46. This evidence concerns the gene IFNA1 and hepatitis C virus infection.