Since the CRPC is a very heterogeneous disease, and in order to more generalize our findings, we sought to employ PCa cell lines that had acquired resistance to therapeutic agents that target the AR axis [19,20], including (i) three subclones from the LNCaP cells which mimic hormone ablation-resistance (LNCaP-abl), are resistant to abiraterone acetate (LNCaP-Abi), or to apalutamide (LNCap-ARN509) and (ii) one C4-2B subclone which is resistant to enzalutamide (C4-2B-ENZA). This evidence concerns the gene AR and posterior cortical atrophy.