The metabolic cancer shift occurs in response to a range of genetic alterations combined with the dysregulation of critical transcription factors and/or oncogenic tumour pathways–as MYC, hypoxia-inducible factor-1 alpha (HIF-1α), nuclear factor kappa-light-chain-enhancer of activated B cells (NK-κB), tumour suppressor p53, and phosphatidylinositol 3 Kinase/Akt/Mammalian Target of Rapamycin (PI3K/Akt/mTOR) pathway [14,15,16] (Figure 1). The gene discussed is AKT1; the disease is neoplasm.