KLK2 can activate protease-activated receptors (PARs)on the surface of neighboring fibroblasts, which in turn release cytokinesthat stimulate PCa cell proliferation,11 while in the bone microenvironment KLK3 promotes osteoprogenitorcell proliferation and osteoblast differentiation and establishmentof bone metastases.12,13 More recently, KLK14 has alsobeen implicated in CRPC development; while KLK14 is normally suppressedby AR signaling (Figure 1A), treatment with AR-targeted drugs may increase KLK14 expressionto promote PCa cell migration and bone matrix colonization.14,15. The gene discussed is KLK14; the disease is posterior cortical atrophy.