The possible explanations could be that: 1) elevated TNF‐α, IL‐1β, IL‐6, and IL‐17A could regulate indoleamine 2,3-deoxygenation enzyme-1 and consequently modulate 5-hydroxytryptamine, the latter one is involved in the pathogenesis of anxiety and depression (24-, 26): 2) pro-inflammatory cytokines could accelerate neuronal damage, which further leads to cognitive impairment (22,23). The gene discussed is IL17A; the disease is depressive symptom measurement.