Newborn Nestin-TVA mice were co-infected with viral vectors of KRas, Tet-off and TRE-Akt (TRE is a tet-responsive element), and the delivered Akt expression was controlled by the Tet (tetracycline) system; tumor formation began to be seen at three weeks of age; suppression of Akt expression with an AKT inhibitor (doxycycline) significantly decreased cell proliferation, regressed tumor size, and extended mice survival, further revealed that tumor progression and maintenance required AKT expression [41]. This evidence concerns the gene AKT1 and neoplasm.