After a stroke, TNF-α amplifies the Glu release cascade through SDF-1α/CXCR4, increases neuronal excitotoxicity, promotes the continuous release of pro-inflammatory mediators (TNF-α, IL-1β, and IL-6) from microglia and astrocytes, and positively feedback regulates the neuroinflammatory microenvironment [86, 87]. The gene discussed is IL1B; the disease is stroke disorder.