Urologic diseases, including benign and malignant conditions, impose a major global health burden.1 However, therapeutic development remains limited by an incomplete understanding of causal molecular drivers.2 Here, we performed a genome-wide Mendelian randomization analysis integrating blood-derived expression quantitative trait loci (eQTL) with genome-wide association study (GWAS) data, focusing on druggable genes with cis-eQTL evidence to systematically prioritize and validate therapeutic targets for urologic diseases (Fig. S1). Through two-sample Mendelian randomization, we identified genes with putative causal roles in urologic diseases, including leukocyte receptor tyrosine kinase (LTK) for bladder cancer and cyclin A2 (CCNA2) for benign prostatic hyperplasia (BPH). Functional annotation revealed key pathways and protein–protein interaction networks relevant to disease pathogenesis. Both genes demonstrated potential clinical relevance in external datasets. These findings provide genetically supported targets with translational potential and may contribute to the development of more effective treatment strategies for urologic diseases.