The chronic inflammation in RA is caused by the overproduction of various proinflammatory cytokines, which results in an excessive activation of T and B cells, with an uncontrolled production of autoantibodies targeting self-antigens or post-translationally modified molecules, such as rheumatoid factor (RF) or anti-citrullinated protein antibodies (ACPA) [4,6,7], that are involved in RA pathogenesis [8]. The gene discussed is PRTN3; the disease is rheumatoid arthritis.