Inflammatory cytokines, including interleukin-1 (IL-1), tumor necrosis factor-α (TNF-α), and interferon-γ (IFN-γ), affect the differentiation and proliferation of erythroid progenitor colony formation in vitro [2–4]; the proapoptotic effects of which have been reversed by treatment with the TNF-inhibitor infliximab in patients with rheumatoid arthritis [5, 6]. The gene discussed is TNF; the disease is rheumatoid arthritis.