In the case of non-selective quinazoline α1-AR antagonists, which are prescribed to treat benign prostatic hyperplasia (BPH) through the relaxation of smooth muscle, this review will highlight their ability to activate PGK1, a non-α1-AR-mediated mechanism, to increase glycolysis to remediate neurodegenerative diseases. The gene discussed is PGK1; the disease is benign prostatic hyperplasia.