Abstract
Benign prostatic hyperplasia (BPH) is a prevalent condition in aging men with significant genetic underpinnings. Twin studies suggest a heritability estimate ranging from 40%-70%, and historic segregation analyses suggest possible autosomal dominant heritability pattern. However, no single gene mutation has been identified and validated as a common cause of lower urinary tract symptoms/BPH. Genome-wide association study approaches have identified numerous low-effect variants that contribute to polygenic risk of BPH. This article integrates recent advances in BPH genetics with clinical insights and outlines future research directions for personalized risk stratification.