We also showed that EE significantly increased the expression of astrocytic HMGB1 in the ischemic hemisphere, which has been shown to be able to promote peri-infarct angiogenesis and functional recovery in the delayed phases of stroke recovery.12 Our further results showed that administration of HMGB1 inhibitor glycyrrhizin increased PSD and PSA in EE mice, and attenuated the promoting effects of EE in angiogenesis and functional recovery in the delayed phases of stroke recovery. The gene discussed is HMGB1; the disease is stroke disorder.