Previous studies have reported that TLR4-mediated signaling causes JNK, p38 MAPK, and NF-κB activation, which induces the production of pro-inflammatory factors, including iNOS, COX-2, TNF-α, and IL-6, in the ischemic area, further exaggerating BBB disruption and cerebral infarction. The gene discussed is NFKB1; the disease is cerebral infarction.