As consequence of these genetic dysfunctions both endocrinological alterations—e.g., HPA axis changes (81) and leptin alterations (65)—and immunological aberrations—e.g., elevated immune activity (82, 83)—are responsible for the disorder observed at the level of monoamines in depression—e.g., noradrenergic and serotonergic neurotransmission alterations (65, 84), being a BDNF modulation suggested as link between the endocrino-immunological alterations and the depressive phenotype (65). The gene discussed is LEP; the disease is depressive symptom measurement.