AKT1 and breast carcinoma: The overexpression of glucose transporter type 3 (GLUT3) in non-malignant breast cancer cells can enhance the activation of epidermal growth factor receptor (EGFR), MAP kinase-activated protein kinase (MAPK), RAC-beta serine/threonine-protein kinase (Akt), and other signaling pathways as well as improve glucose metabolism and the expression of related oncogenes, thereby increasing the risk of cell transformation [31].