Molecular docking and dynamic analysis suggested potential targets (IL17RA and TNFR1) for Emodin in modulating breast cancer development in hyperlipidemia microenvironment.<h4>Conclusion</h4>Emodin effectively reduced tumorigenesis in HFD mice, accompanied with inhibited IL-17 expression and suppressed macrophage infiltration. The gene discussed is IL17A; the disease is breast cancer.