In the last years, B cells have been shown to play a key role in the pathogenesis of rheumatoid arthritis (RA), as suggested by rheumatoid factor (RF) and anti-citrullinated peptide antibody (ACPA) positivity as marker of disease severity that may precede the onset of symptoms by many years [1–4]; moreover, B cell depletion therapy has proven to be effective in seropositive patients [5]. This evidence concerns the gene PRTN3 and rheumatoid arthritis.