PD-L1 on somatic cells interacts with PD-1 on the cytotoxic T cells and inactivates them.38 PD-1/PD-L1 dysregulation involves the pathogenesis of autoimmune diseases, including rheumatoid arthritis and multiple sclerosis.39 40 In SLE, higher percentages of PD-1+CD4+ T cells, PD-1+TIM-3+ NKs and PD-1+ follicular helper-like T cells are identified than in the HCs which may attribute to accumulation of autoreactive T cells.41–44 Our results revealed higher percentages of PD-1+ αβ T cells in the patients with SLE than those in the HCs (figure 2A). The gene discussed is HAVCR2; the disease is systemic lupus erythematosus.