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. Here, NFKB1 is linked to brain ischemia.