Nie et al. also explained that YPFS could ameliorate atopic dermatitis by inhibiting the TLR4/MyD88/NF-κB pathway through animal experiments, and molecular docking showed that compounds such as calycosin, formononetin, and divaricatol had specific binding properties with TNF-α, IL-6, and TLR4 [33]. The gene discussed is TLR4; the disease is atopic eczema.