By reducing mitochondrial ROS production optimizing substrate flexibility, and enhancing glycolysis, UCP2 overexpression can confer a survival advantage in the context of metabolic and oxidative stress127,133,134.On the other hand, cancer cell mitochondria are known to be hyperpolarized—with membrane potentials averaging ~−220 mV, compared to ~−140 mV in non-transformed cells155–157. Here, UCP2 is linked to cancer.