The pathogenesis of sepsis is attributable, at least in part, to dysregulated systemic inflammatory responses characterized by the excessive accumulation of various proinflammatory mediators, such as tumor necrosis factor (TNF) or interleukin (IL)-1 [2], interferon-gamma (IFN-γ) [3], and nitric oxide (NO) [4]. This evidence concerns the gene IL1B and Sepsis.