It has been demonstrated that HIF‐2α mediates the adaptive response to hypoxia in tumor cells. A well‐known example of this is found by Swethajit et al. [11], who concluded that HIF‐2α enhances c‐Myc transcriptional activity (HIF‐2+) and promotes tumor growth by maintaining low levels of glycolysis, allowing for more mitochondrial metabolism and tolerance to ROS‐induced DNA damage for a more oxidative phenotype. The gene discussed is EPAS1; the disease is neoplasm.