As a member of the pattern recognition receptor family, TLR4 plays a critical role in immune responses and phagocytic function.[33] Numerous studies have shown that TLR4 deficiency exerts neuroprotective effects by reducing post‐stroke inflammation.[34, 35] Additionally, our findings indicated that MRP14 triggers mitochondrial dysfunction through TLR4, thereby reducing the energy supply needed for microglial phagocytosis of neutrophils following tMCAO. Here, S100A9 is linked to stroke disorder.