Our data confirmed that Con A activated the TLR4/NF-κB signaling pathway by upregulating the expression of TLR4 and the phosphorylation of IKBα, while the application of ginsenoside CK reversed this state, indicating that ginsenoside CK improved AIH in mice caused by Con A by regulating the TLR4/NF-κB signaling pathway (Figure 6E,F). The gene discussed is NFKB1; the disease is autoimmune hepatitis.