TP53 and neoplasm: Specifically, phosphoinositide 3-kinases (PI3K), Ak transforming factor (Akt) and MYC proto-oncogene (MYC) are known to upregulate transcription and translocation of Glucose transporter 1, and increase hexokinase activity.35,36 P53, possibly the most well-known tumour suppressor gene in the field of oncology, has also been associated with metabolic remodelling, since a loss of P53 results in increased glycolytic flux.37