Endotoxemia in response to bacterial lipopolysaccharide (LPS) is characterized by the production of inflammatory cytokines such as tumor necrosis factor alpha (TNF-α), interleukin 1 (IL-1), and gamma interferon (IFN-γ) along with the release of highly reactive oxygen and nitrogen intermediates which are thought to contribute significantly to the end stage tissue damage in this disease [1–3]. The gene discussed is IFNG; the disease is serum lipopolysaccharide activity.