Recently, tregalizumab, a mAb targeting CD4 on regulatory T cells in RA, failed clinical trials because the high levels of Trx in RA patients reduced a disulfide bond in CD4, which in turn decreased the activity of tregalizumab (29), so it is not without precedent that Trx or other oxidoreductase enzymes could reduce some of the many disulfide bonds in therapeutic mAbs. The gene discussed is TXNRD1; the disease is rheumatoid arthritis.