In addition, the transcriptional activity of leukocytes (CD19+CD3− B cells and CD3+CD4+ T cells) was higher in SLE patients than in healthy controls [7], suggesting the prolonged upregulation of nucleic-acid-sensing pathways could change the immune effector functions and induce a systemic inflammation observed in SLE pathogenesis. The gene discussed is CD4; the disease is systemic lupus erythematosus.