Differences in glutamine metabolism have been shown for MYC-driven liver and lung tumours,84 and branched-chain amino acid metabolism for tumours induced by KRAS activation and TP53 (KP) deletion in lung and pancreas.85,86 Evaluating metabolic gene expression patterns in prostate cancer samples also demonstrated that, in contrast, to samples with high MYC levels, samples with high levels of phosphorylated AKT (pAKT) had increased levels of glycolytic genes.87 This was consistent with the levels of expression of glucose transporter 1 (GLUT1) in these samples. The gene discussed is MYC; the disease is Familial prostate cancer.