In a recent mechanistic study Liang et al. demonstrated that KD could improve CUMS-induced depression-like behaviors in mice by suppressing glial activation markers (Iba-1 and GFAP), hampering the expression of inflammatory cytokines, including IL-1β, TNF-α, and COX-2, inhibiting the TLR4/MyD88/NF-κB signaling pathway, and promoting the BDNF/TrkB/CREB and Wnt/β-catenin signaling pathways [188]. The gene discussed is BDNF; the disease is depressive symptom measurement.