Benign Prostatic hyperplasia (BPH) - a hyperproliferative pathology of the adult prostate leading to morbidity and increased healthcare costs, is a common condition affecting about half of all men aged 50 years and above. Currently, treatments are limited to 5-alpha reductase inhibitors and/or alpha-blockers, which commonly fail. Therefore, there is an urgent need for identifying new alternative molecular-based therapies for effective management of BPH. We integrated RNA-seq data from three independent BPH patient cohorts to identify a common BPH transcriptome. Further, connectivity map analysis of the common BPH transcriptome revealed NSC23766, a small molecule inhibitor of TIAM1 signaling pathway, as a potential candidate compound for BPH therapy. Treatment of epithelial and stromal cell line models of human BPH with NSC23766 led to decreased cell proliferation. Using NSC23766 as a proof-of-concept inhibitor of the TIAM1 signaling, we are currently investigating the cellular and molecular mechanisms that are regulated by TIAM1 signaling in BPH. To achieve this goal, we plan to perform an unbiased RNA seq analysis of NSC23766-treated human BPH cells. Results will reveal the potential molecular/signaling pathways that are regulated by TIAM1 signaling in human BPH.