These animal and cellular model studies, together with genetic studies that revealed AD to be associated with polymorphism in ABCA1 [189, 190] as well as with the related transporter ABCA7 [191], suggest that apoE4 is lipidated less effectively by ABCA1 and that the resulting hypolipidated apoE4 plays an important role in mediating the pathological effects of apoE4. The gene discussed is APOE; the disease is Alzheimer disease.