PCa can be characterized by four predominant genetic and cellular modifications which include the presence of the TMPRSS2-ERG gene fusion [1]; loss of phosphatase and tensin homolog (Pten) tumor suppressor function ultimately resulting in constitutive PI3K-pathway activation [2]; amplification of the oncogene Myc[3]; and the amplification, over-expression or mutation of the AR [4], [5]. This evidence concerns the gene PTEN and posterior cortical atrophy.