Despite the seemingly redundant functions of LXRα and LXRβ in promoting cholesterol efflux after ligand activation, only the LXRα knockout (Lxrα−/−) mice bred to the Apoe−/− or Ldlr−/− backgrounds increased aortic lesions, which suggested that basally LXRβ was unable to compensate for the loss of LXRα to help prevent atherosclerosis [90,91]. This evidence concerns the gene LDLR and atherosclerosis.