The complex pathophysiology of RA cannot fully be captured by either of these antibodies (RF or ACPA) alone because not all patients have RF-positive or ACPA-positive disease, and it has been shown that other autoantibodies, such as anti-carbamylated protein antibody, are involved [9, 10], which also demonstrates the active role of antibody-mediated (i.e. humoural) autoimmunity. Here, PRTN3 is linked to rheumatoid arthritis.