The pathogenesis of sepsis is attributable, at least in part, to dys-regulated systemic inflammatory responses characterized by excessive accumulation of various proinflammatory mediators such as interleukin (IL)-1 [2], interferon (IFN)-γ [3], nitric oxide [4], [5], and macrophage migration inhibitory factor (MIF) [6]. The gene discussed is IL1A; the disease is Sepsis.