According to the monoamine hypothesis, the pathophysiological basis of depression is a deficit in monoaminergic transmission in the central nervous system (Delgado, 2000; Hirschfeld, 2000), whereas the BDNF theory emphasizes that depression is owing to dysfunctional neurogenesis in brain regions responsible for emotions and cognition (Duman and Monteggia, 2006); that is, the expression of neuronal growth factors decreases when we perceive a stress effect (Kim et al., 2020). The gene discussed is BDNF; the disease is depressive symptom measurement.