Targeting Gls1 had a therapeutic effect on experimental autoimmune encephalomyelitis (EAE) and rheumatoid arthritis, mainly by decreasing Th17 and Th1 responses and increasing the Treg response.19, 20, 21, 22, 23 We found that the inhibition of Gls1 by BPTES induced a significantly increased Treg response and decreased Th1 and Th17 responses in both a circulatory immune organ (spleen) and a local immune organ (MLN) compared with the control. The gene discussed is GLS; the disease is rheumatoid arthritis.