In contrast to normal immune response, for example to viral infections, where TLRs can discriminate self-derived DNA from microbe-derived DNA, in patients with SLE the regulation of nucleic sensing and pathways triggering activation of type I IFN production is disturbed and SLE patients exhibit abnormally high levels of INF-α in their blood correlating with more severe disease manifestations (217, 218). This evidence concerns the gene IFNA17 and systemic lupus erythematosus.