An important observation we made is that, in contrast to wild type mice, 12-weeks administration of ritonavir (5 mg/kg/day) to ApoE−/− mice failed to exacerbate the dyslipidemic phenotype of these mice and that, while pharmacological treatments were effective in protecting against accelerated atherosclerosis, both the FXR and PPARα ligand had no effect on serum lipoprotein profile. The gene discussed is NR1H4; the disease is atherosclerosis.