Several genomic alterations in particular represent attractive targets associated with resistance and/or sensitivity to specific PCa treatments, including (i) phosphate and tensin homolog (PTEN) loss resulting in PI3K/AKT activation;(ii) MYC amplification correlated with metastatic phases of the disease, and finally with poor prognosis; (iii) AR mutations related to resistance hormonotherapy; (iv) TMPRSS2-ERG gene fusion; and (v) a deficiency in DNA repair genes responsible for more aggressive PCa features and worse survival (29). Here, AR is linked to posterior cortical atrophy.