As a trigger of inflammation and the dysregulated host response in sepsis (Salomao et al., 2012), circulating LPS is known to induce extensive pro-inflammatory cytokine expression including TNF-α, IL-1β, and IL-6, which contribute to the pathophysiology of endotoxic shock such as tissue injury, capillary leakage, circulatory failure, and multiorgan dysfunction (Van Amersfoort et al., 2003). This evidence concerns the gene IL1B and Sepsis.