To test this hypothesis, the TP53 gene was sequenced in all the healthy controls’ (n = 47) DNA samples; four (8.5%) had the homozygotic WT variant, 19 (40.4%) had the heterozygotic variant, and 24 (51.1%) individuals had the homozygotic mutated variant, showing no connection with BPH development. This evidence concerns the gene TP53 and benign prostatic hyperplasia.