During the cerebral ischemia‐reperfusion process, endogenous ligands activate nuclear factor‐κB (NF‐κB) through the TLR4 signaling pathway, and induce the production of a large number of proinflammatory factors, chemokines, adhesion molecules, and other molecules to produce inflammatory cascades that exacerbate brain tissue damage.8 The gene discussed is NFKB1; the disease is Cerebral ischemia.