The rat experiment showed that after 4 hours of focal ischemia caused by acute ischemic stroke, the serum ACE2 activity initially decreased, and then rebounded within 3 days.[40] Preclinical studies on acute ischemic stroke indicated that the activation of ACE2/Ang (1–7)/Mas axis through targeted intervention could induce neuroprotective effects.[41] Bennion et al[27] showed that serum ACE2 activity was significantly correlated with ischemic stroke, but did not correlate with the infarction area of stroke. The gene discussed is ACE2; the disease is infarction.