Studies have shown that ATP is reduced in the urothelium of BPH patients with detrusor underactivity,[80] while ATP hydrolysis disorder reduces adenosine A1 receptor-mediated inhibition of cholinergic nerve activity in BPH patients with bladder outlet obstruction.[81] However, there is no direct study of Stepholidine and Adenosine triphosphate applied in the treatment of BPH, and the findings of this study may provide some new chemical components and targets for the treatment of BPH. This evidence concerns the gene ADORA1 and benign prostatic hyperplasia.