Accordingly, in the cerebral arterioles of hypercholesterolemic female mice, endothelium-dependent dilator responses are improved by treatment with the cell permeable SOD mimetic tempol, a superoxide scavenger, and apocynin, an inhibitor of NADPH oxidase [109], suggesting that hypercholesterolemia may modulate cerebral arteriolar dysfunction, at least in part, via NADPH oxidase-derived •O2-. The gene discussed is FMO5; the disease is familial hypercholesterolemia.