The deficiency of Tregs can be promoted by low-dose interleukin-2 (Ld-IL2).12,13 A study showed that defects of Tregs from patients with RA were reversed by exogenous IL-2 in vitro.14 On the other hand, Ld-IL2 can inhibit Th17 cell proliferation, which is associated with the development of RA.15 Ld-IL2 treatment may be beneficial in RA. The gene discussed is IL2; the disease is rheumatoid arthritis.