Sustained up-regulation of the class I PI3k-Akt-mTOR axis in ovarian cancers may arise from activating mutation or duplication of genes coding for the Tyrosin Kinase Receptors EGFR and PDGFR, for PI3kCA or Akt[65,66], as well as by inactivating mutations of PTEN[67] or hyper-expression of the PTEN-regulator protein DJ-1[68]. The gene discussed is AKT1; the disease is ovarian carcinoma.