Indeed, Qin et al. demonstrated that N-acetylcysteine-dependent ROS scavenging diminished NF-κB and HIF-1α activation in autophagy-deficient GC cells, preventing the metabolic switch (from mitochondrial oxidative phosphorylation to aerobic glycolysis), which is closely associated with malignity and chemoresistance in GC [111]. Here, HIF1A is linked to gastric cancer.