However, in autoimmune diseases, such as rheumatoid arthritis, TLOs have been shown to support local autoantibody responses (e.g., rheumatoid factor, ACPA/anti-CCP) linked with disease exacerbation and also influence the clinical response to mainstream biologics (e.g., anti-TNF) (4, 7–9). The gene discussed is PRTN3; the disease is rheumatoid arthritis.