However, it was reported that although peripheral Tregs in RA patients are capable of suppressing the proliferation of effector T cells, they were unable to suppress the production of pro-inflammatory cytokines (TNF, IFN-γ) by monocytes and activated T lymphocytes, whereas therapy with anti-TNF immunoglobulins completely restored the Treg function [63]. The gene discussed is IFNG; the disease is rheumatoid arthritis.