In particular, anti-C1s antibody sutimlimab significantly inhibited Ig-induced activation of B cells derived from patients with rheumatoid arthritis, indicating that targeting C1s may not only block complement-mediated tissue damage, but also suppress the activation of autoimmune B cells, which is a critical pathogenic factor in many autoimmune diseases (13). The gene discussed is C1S; the disease is rheumatoid arthritis.