We previously found that relative to those who used tamsulosin or no α1-adrenergic antagonist, people with PD who used TZ/DZ/AZ had slower progression of motor dysfunction and reduced PD-related complications.22 For the subset of patients with PD for whom impaired energy metabolism played a pathogenic role, these results suggested that the neuroprotective effect of enhancing PGK1 activity and glycolysis might prevent development or delay PD. The gene discussed is PGK1; the disease is Parkinson disease.