Pharmacological studies have found that arctigenin (AG) and ginsenoside Rh2 (GRh2) can ameliorate host or host offspring MDD caused by T. gondii infection, mainly because AG and GRh2 can inhibit microglia activation and neuroinflammation via the TLR4/NF-κB, TNF receptor 1 (TNFR1)/NF-κB signaling pathways and high mobility group box 1 (HMGB1)/TLR4/NF-κB signaling pathway, respectively (Cheng et al., 2020; Xu et al., 2022). The gene discussed is NFKB1; the disease is major depressive disorder.