A pathophysiologic role is supported by the very early induction of ACPA and anti-CarP antibodies in RA, often long before the disease becomes clinically manifested, the more severe progression of the disease in seropositive patients, the induction of arthritis in animal models upon immunization with citrullinated antigens, and the exacerbation of arthritis by ACPA in murine models of arthritis (12). Here, PRTN3 is linked to arthritic joint disease.