The host response against a bacterial infection that leads to a systemic inflammatory response syndrome is defined as sepsis, which is characterized by the increase in TNF-α, IL-1β, IL-6, and IL-8 cytokine secretion mainly by macrophages after the recognition of bacteria or bacterial-derived lipopolysaccharide (LPS) via TLRs [21, 160]. This evidence concerns the gene IL1B and Sepsis.