Thus we selected candidate genes a priori based on: i) evidence of role in depression in animal models and also in our previous human studies, ii) having functional polymorphisms if possible, and iii) directly or indirectly influencing the main putative pathways of depression, including serotonin, HPA, neuropeptide, neurotrophin, endocannabinoid, and neuroinflammatory mechanisms. This evidence concerns the gene NPS and depressive symptom measurement.