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]. The gene discussed is AR; the disease is neoplasm.