These findings indicate that pathogenic Th17 and Th17.1 may exacerbate immune diseases through the ABA treatment-mediated inhibition of the co-stimulatory signals from CD28 and co-inhibitory signals from CTLA-4 in patients with RA, although we did not investigate CTLA-4 levels on Th17.1, which is a limitation of this study. The gene discussed is CD28; the disease is rheumatoid arthritis.