The results presented here may support our hypothesis that evolutionary substitutions of two amino acids (from 130Glu/136Asn to 130Gly/136Thr) during early human evolution decreased monoamine uptake of VMAT1 and promoted increased levels of anxiety, depression, and neuroticism, given several lines of evidence for association of the 130Gly/136Thr variant with neuropsychiatric phenotypes. The gene discussed is SLC18A1; the disease is depressive symptom measurement.