This finding is consistent with that of a recent randomized clinical trial that compared targeted low-normal (65–75 mmHg) and high-normal MAP (80–100 mmHg) in 123 comatose cardiac arrest patients [44], in which despite a clear separation in MAP between the two MAP target groups, the regional cerebral oxygen saturation (measured by using NIRS monitoring), neurobiomarkers (neuron-specific enolase and S100B), and clinical outcomes did not differ between the two groups. The gene discussed is S100B; the disease is cardiac arrest.