In Alzheimer's disease (AD) much attention has focused on how cholesterol influences the enzymes which process the amyloid precursor protein (APP) and in particular that high cellular cholesterol shifts APP processing towards production of the amyloid β peptide (Aβ), which in turn accumulates in neuritic plaques, while lower cellular cholesterol levels promote α-secretase cleavage of APP and prevent Aβ formation [3]. The gene discussed is APP; the disease is Alzheimer disease.