Previous studies have suggested that increased Tfh cell responses in RA are driving B cell autoantibody production, therefore, the increased availability of Tfh cells in ACPA+ over ACPA− RA patients could be implicated in the generation of ACPA, however, further studies are required in order to elucidate the Tfh-autoreactive B cell interactions in RA [32,33]. This evidence concerns the gene PRTN3 and rheumatoid arthritis.