As for HMGB1’s role in neuroinflammation, short hairpin-mediated HMGB1 knockdown or HMGB1 monoclonal antibody-mediated inhibition of HMGB1 during the hyperacute phase after stroke inhibited increased blood–brain barrier permeability, microglia activation, inflammatory factor release, and iNOS expression [126, 133]. Here, HMGB1 is linked to Stroke.