Always Awake (IMAGE) University of Pennsylvania School of Medicine Caption Oncogenic MYC disrupts the molecular clock and alters circadian glucose metabolism and glutaminolysis in favor of growth-related biosynthesis in cancer cells. Both MYC and N-MYC upregulate REV-ERBa, which suppresses BMAL1 expression and oscillations. High REV-ERBa or low BMAL1 predicts poor clinical outcome in N-MYC-driven human neuroblastomas. Credit Perelman School of Medicine, University of Pennsylvania; <em>Cell Metabolism</em> Usage Restrictions None License Licensed content Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.