IFN-γ, as a pivotal proinflammatory cytokine, modulates immune responses and has been implicated in the pathogenesis of sepsis.[15] It has been suggested that dysregulated production of IFN-γ contributes to immune suppression and subsequent susceptibility to secondary infections and organ dysfunction in sepsis.[16] TNF-α, another essential cytokine in sepsis, exerts pleiotropic effects on the immune system and has been linked to the pathogenesis of tissue injury and multi-organ dysfunction in sepsis. This evidence concerns the gene TNF and infection.