Here our results suggest that in depression these factors may converge on intracellular pathways (e.g., MAPK pathway), mitochondria and energy metabolism, and on other neurochemical pathways, such as SAT1 and polyamines [25], resulting in altered function and cell structure (growth, adhesion) within the amygdala-cingulate network (Table 1). The gene discussed is SAT1; the disease is depressive symptom measurement.