Here, we found that removing such chronically high levels of QR2 results in a proteome that is functionally opposed to that seen in AD brains (20), where high QR2 expression levels are found (16, 30), and in which QR2 polymorphisms adversely affect pathology (29), strengthening the case for QR2 inhibition as a therapeutic avenue. The gene discussed is NQO2; the disease is Alzheimer disease.