In line with the results obtained in WT mice, we found that the intestinal activation of Lxrα correlates with an increased accumulation of hepatic triglycerides (Fig. 6A), and a reduction of the relative abundance of polyunsaturated fatty acids specimens (Table 5), thus correlating with the more pronounced liver steatosis observed in iVP16LXRα. The gene discussed is NR1H3; the disease is fatty liver disease.