Considering that performance in reversal learning and set shifting depends on the normal structure and function of the serotoninergic system in the OFC and of the noradrenergic system in the mPFC, respectively [5, 8–10, 62, 63], these results suggest that different components of cognitive flexibility may be regulated by different ERK signaling pathways downstream of stress-induced changes in monoaminergic signaling, which shows extensive deficiencies in depression. The gene discussed is MAPK1; the disease is depressive symptom measurement.