Treatment of a patient harboring a malignant tumor with IFN-α induced SLE-like symptoms (76), and it is also epidemiologically interesting that SLE patients with high IFN-α levels showed low rates of hepatitis B infections (77), highlighting the role of IFN-α not only in antitumor and antiviral responses but also in the pathogenesis of SLE. This evidence concerns the gene IFNA1 and systemic lupus erythematosus.