Proteolytic enzymes, such as prostate-specific antigens (PSAs) and urokinase-type plasminogen receptors (UPAs), can not only promote the growth of tumor, but also disrupt the balance of osteoblasts and osteoclasts by cleaving PTHrP and promoting TGF-β production, respectively [39,40]. The gene discussed is KLK3; the disease is neoplasm.