In agreement with earlier reports showing that hypoxia increases mitochondrial O2- production in cancer cells (Chandel et al., 2000; Sabharwal and Schumacker, 2014; Eales et al., 2016) and cultured endothelial cells (Hernansanz-Agustín et al., 2014), we found that exposure to acute hypoxia stimulated ROS generation in native cerebral artery endothelial cells, and that this response was inhibited by a mitochondrial-targeted SOD mimetic and by intracellular PEG-SOD. Here, SOD1 is linked to cancer.