Although further studies are needed to unravel the underlying molecular mechanisms related to these findings, it is possible that they reflect changes in Aβ clearance mechanisms that, depending on the genetic variation, may either enhance or decelerate the disease pathogenesis.Thus, it is possible that AD patients with different APOE and NR1H3 genotypes respond differently to LXRα agonist or other ApoE-related treatments. The gene discussed is NR1H3; the disease is Alzheimer disease.