Several inflammatory and pathogenic pathways in depression have been proposed, such as reduced brain monoaminergic transmission (e.g., serotonin, norepinephrine), increased proinflammatory cytokines (e.g., IL-1, IL-6, IL-17, TNFα), reduced neurotrophic factors, elevated oxidative stress and dysregulation of HPA-axis, which are similar to CFS [50]. This evidence concerns the gene IL17A and depressive symptom measurement.