Endotoxin, a component of the bacterial cell wall, is recognized by Toll-like receptors (TLRs) by the host, which binds this component and triggers activation of the nuclear factor kappa or the NFκB pathway, which in turn stimulates the synthesis and release of pro-inflammatory cytokines (e.g., tumor necrosis factor alpha (TNFα), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6)) and stimulates other aspects of the immune system that increase the intensity of the metabolic response to infection. The gene discussed is TNF; the disease is infection.