Cerebral ischemia stress robustly induces the extracellular release of damage-associated molecular patterns (DAMPs) from necrotic and dying neural cells within ischemic territory, which may function as the endogenous ligands for TLR4 and induce the activation of TLR4/nuclear factor κB (NF-κB) signaling pathway, thereby enhancing both innate and adaptive immunity and promoting post-ischemic neuroinflammation and brain infarction [6,7]. The gene discussed is TLR4; the disease is brain infarction.