Whereas ET1 level falls significantly in the white matter in Alzheimer’s disease, presumably as a physiological adaptation to reduced blood flow, it rises significantly in the cerebral cortex (Palmer et al., 2012) and leptomeningeal blood vessels (Palmer et al., 2013); as we reported previously, this is probably in response to locally elevated amyloid-β and oxidative stress. The gene discussed is EDN1; the disease is Alzheimer disease.