Since the activation of immunoglobulin-like transcript 7 (ILT7), a receptor molecule expressed on the surface of pDCs [94], leads to downregulation of TLR7/TLR9-mediated IFN production, by inducing a preferential differentiation of pDCs to an APC phenotype [94,95], stimulation of ILT7 has been regarded as a potential therapeutic option in patients with autoimmune diseases characterized by type I IFN signature. The gene discussed is TLR7; the disease is autoimmune disease.