Dang et al found that KXS can reduce the expression of AChE in the hippocampus, increase concentrations of various monoamine neurotransmitters in the hippocampus and PFC and reduce the concentration of serum ACTH, significantly improving the depression symptoms in mice subjected to CMS.89 KXS was found to ameliorate 5‐HT defects, which is achieved by raising the synthesis, inhibiting the reuptake and ultimately increasing the concentration of intracephalic 5‐HT.90, 91 In an earlier study, impacts and potential mechanisms of KXS2012 on depression in both cell and animal models were validated. The gene discussed is ACHE; the disease is major depressive disorder.