HIF1A and cancer: The induction of HIF1-α and ATF4 in response to limiting nutrient conditions, results in the upregulation of glucose and amino acid transporters, which helps cancer cells to compete for various nutrients24; HIF1-α also induces the expression of glycolytic enzymes, thereby facilitating sustained ATP production.25 Oncogenic driver mutations, such as those in c-Myc, can result in the aberrant activation of mammalian target of rapamycin complex (mTORC)-1, which promotes nutrient uptake and the anabolic conversion necessary for cell growth and division.26