Innovatively, on one hand, the expression level of heat shock protein (HSP70) increased obviously and was participated in the upregulation of soluble cytoplasmic DUSP8 levels, which induced by cerebral ischemia; on the other hand, inhibition of the activity of HSP70 by using quercetin led to restore the activation of JNK via downregulating the cytoplasmic solubility of DUSP8, suggesting DUSP8 involved in the process of inactivating JNK activation in response to cerebral ischemia required the molecular chaperon HSP70 to impetus the calibration of folding defects [65]. The gene discussed is DUSP8; the disease is Cerebral ischemia.