Since blockade of TNFR2 in the presence of exogenous TNF-α restores the basal levels of IFN-γ and IL-17-producing Th1 and Th17 cells, as observed herein, we believe that targeting TNFR2 with a blocking antibody may represent an alternative strategy to normalize the levels of RA-associated cytokines, thus preventing the harmful effects of TNF-α in this disease, especially in patients that do not respond adequately to TNF-α antagonists. The gene discussed is TNFRSF1B; the disease is rheumatoid arthritis.