Molecular docking confirmed that simvastatin forms stable complexes with TLR2, CCR1, and CCL4, potentially exerting multi-target effects in AS: beyond inhibiting HMG-CoA reductase for lipid lowering, simvastatin may suppress NF-κB-mediated inflammation via TLR2,[42,43] disrupt immune cell recruitment through the CCR1-CCL4 axis, and reduce oxidative stress.[44,45] As an FDA-approved drug with established safety in cardiovascular disease, simvastatin represents a promising candidate for repurposing in AS. The gene discussed is CCL4; the disease is cardiovascular disorder.