This classic model begins with isolated autoantibody positivity (seropositivity) for rheumatoid factor (RF) or often much earlier anti‐citrullinated peptide antibodies (ACPA), followed by a transition to inflammatory‐type joint pain without visible synovitis (clinically suspect arthralgia) and finally the onset of clinically evident arthritis.16 This evidence concerns the gene PRTN3 and Arthritis.