Most PCs are usually acinar adenocarcinomas characterized by glandular formation, absence of basal cells, uncontrolled proliferation of tumor cells, and expression of differentiation luminal markers, such as the androgen receptor (AR) and the prostate-specific antigen (PSA), and the majority of these adenocarcinomas are androgen-dependent, which allows hormone therapy that inhibits AR signaling [1,2,3,4]. Here, KLK3 is linked to neoplasm.