The potentiation of Aβ clearance by degradation, and the subsequent amelioration of AD hallmarks, has recently been demonstrated in vivo by inducing the transcription and lipidation of apoE through treatment with an agonist for the liver X receptors, in combination with the further induction of the transcription of apoE and the reduction in the microglial expression of proinflammatory genes through treatment with an agonist of the peroxisome-proliferator receptor γ [48]. This evidence concerns the gene APOE and Alzheimer disease.