Emerging evidence suggests that the CUMS model of depression can induce depressive-like behaviors, peripheral and central inflammation, neuronal cell damage, hyperactivity of the hypothalamic–pituitary–adrenal axis (HPA), increased hippocampal apoptosis, decreased neurogenesis, and reduced BDNF and 5-HT1A levels (Czeh and Di Benedetto, 2013; Yirmiya et al., 2015). This evidence concerns the gene HTR1A and depressive disorder.