The accumulation of oxysterols in APOE4 and AD promotes increased expression of ABCA1 and caveolin-1, leading to the endocytosis and sequestration of ABCA1 in lysosomes and the induction of a dysfunctional lysosomal state, in which ABCA1 cannot be recycled back to the plasma membrane [118]. The gene discussed is APOE; the disease is Alzheimer disease.