AR and benign prostatic hyperplasia: DHT is predominantly generated by 5α-reductase (5αR) from testosterone; it binds androgen receptors with high affinity, and the DHT–androgen receptor complex initiates the transcription and ultimately regulates the cell cycle, cell growth, and differentiation of prostate stromal and epithelial cells to promote enlargement of the prostate and BPH pathogenesis [29].