For instance, Su et al. demonstrated that metabolic and subsequent MES reprogramming in GBM occurs through the TGFβ1-mediated upregulation of NADPH oxidases 4 (NOX4) and reactive oxygen species (ROS), leading to downstream overexpression and nuclear accumulation of hypoxia-inducible factor 1α (HIF-1α) [93]. The gene discussed is HIF1A; the disease is glioblastoma.