Since the inhibition of TNF-α may predispose to failure to maintain the chronicity of the disease, with the consequent conversion of bradyzoites into tachyzoites due to the impairment of anti-T. gondii immune response [16,22], our study evaluated cellular markers and the production of important cytokines for controlling the parasite in patients with rheumatic diseases using TNF antagonists. The gene discussed is TNF; the disease is rheumatic disorder.