Once the relevance of CLDN3 silencing in a CRPC model was demonstrated, we further investigated CLDN3 expression in samples from patients with benign prostatic hyperplasia (BPH), primary tumors that did not develop resistance to androgen deprivation (androgen-sensitive prostate cancer HS-PC), and tumors that progressed afterwards to CRPC. This evidence concerns the gene CLDN3 and benign prostatic hyperplasia.