As a result of cerebral ischemia, TLR4 regulates the levels of inflammatory mediators and promotes downstream signalling, including activation of the nuclear factor kappa B (NF‐κB) transcription factor, which then interacts with multiple gene promoters and enhancers to influence a wide range of physiological activities, including inflammation, haematogenesis, immune response, cell proliferation and programmed cell death, which ultimately induces neuroinflammatory responses and injury.11, 12, 13. The gene discussed is NFKB1; the disease is Cerebral ischemia.