Complement system is activated at early time during sepsis, causing C5a production, which may play a central role in generation of “inflammatory cytokine storm.” During sepsis, there is an increase of both pro-inflammatory mediators in blood including IL-6, TNF-α, IL-1β, IL-8, and IFN-γ, and anti-inflammatory factors such as IL-10, IL-13, IL-4, and TGF-β (Wolkow, 1998; Titheradge, 1999; Le Tulzo et al., 2002; Guo et al., 2004; Flierl et al., 2008b). The gene discussed is IL1B; the disease is Sepsis.