Three non-ATP-competitive allosteric Akt inhibitors (Akt1i, Akt2i, and Akt1/2i) reduced glucose transport into T-47D breast cancer cells, by interfering with a process distinct from the Akt signaling pathway (involved in movement of GLUT4 to the plasma membrane, e.g., in adipocytes). This evidence concerns the gene AKT1 and breast carcinoma.