In summary, this study proposed a complete mechanism model for CEP in the treatment of BPH: CEP binds to the EGFR kinase domain and the PH domain of AKT with high affinity, blocks EGFR dimerization and PI3K membrane recruitment, inhibits AKT phosphorylation and reduces its translocation to the cell membrane. The gene discussed is AKT1; the disease is benign prostatic hyperplasia.