Thereby, ATP produced by the mitochondria decreases under stress while oxygen free radicals increase, affecting the energy supply in the physiological activities of neural cells, and initiates the apoptosis due to releasing cytochrome C and activating Caspase pathway, resulting in the nerve cell disorder [72–74], being supported by the experimental data of cerebral energy metabolism disorder on clinical depression cases and experimental depression animals [75–77]. The gene discussed is CYCS; the disease is depressive symptom measurement.