Considering that KLK1 upregulated the eNOS expression via a BDKRB2-dependent mechanism, we believe that in a similar way to PDE5I, with long-term administration of KLK1, the eNOS/NO/cGMP signal pathway of the prostatic microcirculation could be restored, and then, the endothelial dysfunction and inflammation progression are controlled. Here, KLK1 is linked to endothelial dysfunction.