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. This evidence concerns the gene PIK3CA and benign prostatic hyperplasia.