It has been shown that an increase in p-Akt could inhibit p-GSK3-β via phosphorylation at its N terminus [76], and inhibit p-38 MAPK and NF-κB to reduce depressive-like behaviors by decreasing proinflammatory cytokines in an animal model of depression induced by repeated administration of lipopolysaccharide [73,74,77]. The gene discussed is AKT1; the disease is depressive symptom measurement.