Interestingly, anti-GTF2A2 was the only autoantibody found to be higher in both ACPA+ RA and ACPA − RA; this provides further evidence of previously reported immunological differences between these two subgroups despite sharing similar symptoms5,38, although the precise pathophysiological mechanisms—or potential influences of genetic predisposition39,40—remain yet unclear. This evidence concerns the gene PRTN3 and rheumatoid arthritis.