Consistent with these findings, our previous study demonstrated that treatment with an anti-HMGB1 mAb significantly ameliorated brain infarction in a rat model of middle cerebral artery occlusion by preserving BBB integrity through suppression of microglial activation, TNF-α and inducible nitric oxide synthase expression, and matrix metalloproteinase-9 activity, without altering cerebral blood flow [15]. The gene discussed is MMP9; the disease is brain infarction.