Taken all data together, we suggest that GCJ protects against brain damage and brain dysfunction in animal model ischemia stroke with metabolic syndrome condition via the suppression of DNMT1 and HDAC3 expressions in the cerebral cortex giving rise to the decrease in inflammation [42] via the reduction of IL-6 and TNF-α leading to an improvement of brain infarction area and brain edema together with the neurological deficit. The gene discussed is TNF; the disease is metabolic syndrome.