The potential mechanisms, including the inactivation of CDK [14], disruption of DNA integrity [15], engaging death receptor-mediated caspase-8 activation [16], induction of transforming growth factor-β signaling [17], downregulation of vascular endothelial growth factor [18, 19], and targeting focal adhesion survival signaling [20], have provided molecular underpinnings for the pharmacological exploitation of alpha-1 blocker therapy for a range of epithelial cancers, such as advanced prostate cancer, bladder cancer, and RCC [21]. This evidence concerns the gene PSMA6 and renal cell carcinoma.