The immune response in sepsis has been simplified in two subsequent phases: a cytokine-mediated hyper-inflammatory phase characterized by increased release of pro-inflammatory mediators (such as TNF-α, IL-1, IL-12 and IL-6), which might lead to “cytokine storm” and serious multi-system dysfunction; and a second phase of compensatory anti-inflammatory response, which is facilitated through the release of anti-inflammatory cytokines, such as TGF-β, IL-4 and IL-10, to restore homeostasis [28,29]. The gene discussed is IL1B; the disease is Sepsis.