This was further confirmed in mice with heterozygous loss of PTEN or loss of PTEN lipid phosphatase function (PtenG129E) mouse models that demonstrated AKT hyperactivation in various tissues (17, 61), and in which through the Akt-FRET biosensor we showed spatial up-regulation of AKT in prostate and breast cancer settings. The gene discussed is PTEN; the disease is breast carcinoma.