Whether this mechanism is relevant to RA pathogenesis remains to be determined, but the recent observation that ACPA positivity in RA patients is associated with higher proportions of Th17.1 (IL‐17/IFN‐γ‐double producers) and Th22 cells, but not Th1 and Th2 cells 57 provides tantalizing evidence that this is a possible scenario. Here, PRTN3 is linked to rheumatoid arthritis.