Similarly, a subset of AR-null PCa cellshave high KLK14 expression, which is not perturbed by DHT treatment.15 We hypothesize that these diverse PCa cell populationscontribute to a buildup of KLK activities in the tumor microenvironment.In this study we found that androgen-independent activation of ARin PCa cells by osteoblasts results in an increase of KLK2 and KLK3activity in the bone microenvironment. The gene discussed is KLK14; the disease is neoplasm.