Considering the effect of PD-1 and TIM-3, and the fact that the increased TIM-3+PD-1+ NK cells were associated with disease activity and severity of SLE, it is hypothesized that the increased TIM-3+PD-1+ NK cells may play a role in SLE pathogenesis via other mechanisms, such as serving as a negative feedback mechanism to prevent potential tissue damage caused by excessive autoimmune responses in patients with SLE. Here, HAVCR2 is linked to systemic lupus erythematosus.