LPS binds to toll-like receptor 4 (TLR4) and consequently activates the mitogen-activated protein kinase (MAPK) signaling pathway and induces an NF-κB-dependent inflammatory cascade, resulting in excessive production of proinflammatory mediators (nitric oxide (NO) and prostaglandin E2 (PGE2)) and cytokines (e.g., TNFα and IL-6) that are crucial in mediating the systemic inflammatory response during sepsis [8,9]. This evidence concerns the gene IL6 and Sepsis.