Interestingly, none of these studies showed any significant differences in the mean mRNA expression levels of Akt isoforms between the altered and un-altered groups, suggesting that while genetic alterations in PTEN may have contributed to Akt hyperactivation, there was no evidence on the direct effect of genomic alterations in the Akt1 isoforms on their activity in these PCa samples. Here, AKT1 is linked to posterior cortical atrophy.