This is supported by cases where concurrent treatments that reduce the levels or effectiveness of these cytokines coincide with high parasite burdens, such as: a 57-year-old woman with Crohn’s disease treated with infliximab (a TNF-α-neutralizing monoclonal antibody) with a high level of parasitemia over the course of babesiosis, or a 67-year-old man with severe B. microti infection, who owing to rheumatoid arthritis was being treated with etanercept (a competitive blocker of TNF-α and TNF-β receptors) [162,163]. The gene discussed is TNF; the disease is parasitic infectious disease.