However, chronic oxidative stress drives tumor progression via multiple axes: ROS stabilize hypoxia-inducible factor 1-alpha (HIF-1α), allowing it to upregulate the expression of PD-L1 on tumor cells and thereby inducing T cell exhaustion [8,9,10]; mitochondrial ROS derived from hyperactive glycolysis or Lon protease overexpression reinforce Treg immunosuppression and polarize macrophages toward protumor M2 phenotypes [11,12]; and ROS play important roles in immunosuppressive stromal remodeling [13]. The gene discussed is HIF1A; the disease is neoplasm.