The overexpression of PD-1, PD-L1 and PD-L2 on various immune cells of patients with SLE has been reported, and PD-1 receptors and their ligands have been identified to be involved in two key pathways, the toll-like receptor (TLR) pathway and the type I interferon (IFN-1) pathway through activation of NF-κB and/or STAT1 in the pathogenesis and development of SLE (14, 64). The gene discussed is STAT1; the disease is systemic lupus erythematosus.