Molecular mechanisms that lead to metabolic reprogramming and to the metabolic phenotype of cancer cells are only partly understood and include activation of oncogenes and kinases like c-MYC, members of the phosphoinositide 3-kinase (PI3K) signalling pathway [PI3K, protein kinase B (AKT), mammalian target of rapamycin (mTOR)], stabilization of transcription factors like hypoxia-inducible factor 1 (HIF-1) and inactivation of tumor suppressor genes like p53 [3, 4, 9]. This evidence concerns the gene AKT1 and cancer.