In light of the potential role played by KLK4 (having a sequence homology of 31.64% with thrombin) in prostate cancer via activating either PAR1 or PAR228, we sought to develop a strategy, alternative to generating a KLK4-specific enzyme inhibitor, to prevent KLK4-stimulated activation of PAR1. The gene discussed is KLK4; the disease is prostate carcinoma.