In this context, the transcription of APE1 was shown to be reduced in the entorhinal cortex and mononuclear blood cells of AD patients (Maynard et al., 2015; Lillenes et al., 2016), while the nuclear translocation of APE1 in the cerebral cortex was elevated in another study, as provoked by oxidative DNA damage in response to defective mitochondrial respiration and increased ROS production (Maynard et al., 2015). The gene discussed is APEX1; the disease is Alzheimer disease.