17 Under physiological conditions, these byproducts can be decomposed by antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), or glutathione peroxidase (GPx) to reduce the detrimental effect of ROS as well as control cellular homeostasis.17 However, under different pathological conditions, cells suffering from either ischemia–hypoxia or chemical hazards that disrupt mitochondria function will produce excess ROS, which cannot be efficiently diminished by these antioxidant enzymes, thus leading to oxidative damage. Here, CAT is linked to ischemia.