For instance, the epidermal growth factor receptor (EGFR) tyrosine kinase receptor activates downstream effectors including phosphatidylinositol 3-kinase (PI3K) and AKT signalling.10–14 Further activation of the PI3K–AKT pathway reprogrammes cellular metabolism by augmenting the activity of nutrient transporters and metabolic enzymes, thereby supporting the anabolic demands of aberrantly growing cells.10–14 Genes such as KRAS and c-Myc are commonly amplified/mutated in tumours and frequently influence nutrient uptake and utilisation. This evidence concerns the gene AKT1 and neoplasm.