The E2-induced fibrotic pathways and ECM deposition observed in our study align with observations in various other TGF-β–driven conditions such as dermal fibrosis, systemic sclerosis, benign prostatic hyperplasia, and hepatic fibrosis, underscoring the potential widespread relevance of our findings (45–49). This evidence concerns the gene TGFB1 and benign prostatic hyperplasia.