In sepsis, structural damage to the blood-brain barrier, cerebrovascular endothelial membrane, and surrounding neurons is accompanied by a local response that is translated into an increase in intrathecal cytokine concentrations, enhancing the whole process: increased expression of tumor necrosis factor (TNF)-α, primarily at the periventricular level, and secondly involving glial components with induction of glial expression of interleukin (IL)-1β and IL-6 [28]. The gene discussed is IL1B; the disease is Sepsis.