These and other disadvantages such as delayed onset of efficacy of SSRIs challenge the traditional monoamine-based hypothesis of depression, and emerging evidence favors the neural plasticity hypothesis which proposes an important role of the impaired neural plasticity including neurotrophic factors, cAMP response element binding protein (CREB) signaling, synaptic plasticity influenced by N-methyl-D-aspartate (NMDA) signaling, adult neurogenesis in depression, and neural plasticity as the crucial targets for antidepressant action [6, 7]. This evidence concerns the gene CREB1 and depressive symptom measurement.