To explore a cooperative role for the PI3K-pathway with the MYC oncogene in human prostate cancer, we used existing murine models of human prostate cancer harboring prostate-specific homozygous deletion of PTEN (PTENpc−/− model) [26], [27], or over-expression of either human MYC (Hi-MYC model) [28] or the downstream PI3K-pathway active allele of AKT1 (MPAKT model) [29] and studied the combinatorial effect of these pathways on tumorigenesis. The gene discussed is AKT1; the disease is prostate cancer.