Deposition of β amyloid (Aβ) in hippocampus is of crucial important in the pathogenesis of Alzheimer’s disease (AD). Recent study indicated that it was the decreased Aβ clearance account for its deposition. Studies showed that apolipoprotein E (ApoE) gene is an influential genetic risk factor for sporadic late-onset AD, but the detailed mechanism how it works is not fully understood. An article published in recent issue of Science (2012 Mar) showed that a retinoid X receptor agonist Bexarotene could rapidly activate ApoE, promot Aβ clearance and correct behavior deficits in transgenic AD moue model. These results clearly demonstrate that ApoE promotes Aβ clearance and provide new insight for AD therapy.