These studies revealed that although mutations and deletions in PTEN gene lead to PCa, the lack of difference in mRNA and protein expression (data not shown for Akt2 and Akt3) in the Akt isoforms between the altered and un-altered group indicated that the inhibition of PTEN does not contribute further to the already increased Akt in PCa. The gene discussed is AKT3; the disease is posterior cortical atrophy.