Considering the increased levels of p-AKT1 (Ser473) observed in tumors harboring ETS rearrangements, these observations support the hypothesis that ETS overexpression up-regulates the expression of GRPR and subsequently leads to up-regulation of p-AKT1 (Ser473), placing ETS transcription factors as upstream regulators of GRPR overexpression in PCa. This evidence concerns the gene AKT1 and posterior cortical atrophy.