As it is overexpressed in the prostate tumor site but rapidly inactivated in systemic circulation due to binding to serum protease inhibitors like α2-macroglobulin (A2M) and α1-antichymotrypsin (ACT), PSA is considered an attractive target for small molecule prodrugs against prostate cancer (Lilja et al., 1991; Otto et al., 1998). The gene discussed is KLK3; the disease is prostate cancer.