During endotoxemia, LPS-induced Toll-like receptor 4 (TLR4) activation promotes the expression of proinflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukins (IL-1β and IL-6), and interferon (IFN), via the transcription of nuclear factor-κB (NF-κB), which is a crucial regulator of the immune system [6–8]. The gene discussed is TNF; the disease is serum lipopolysaccharide activity.