Combined treatment by activators of LXR and PPARα exerted a synergistic effect in increasing lipogenesis in the liver via elevating the transcription of acc1, fas and scd1. Consistent with previous studies by Grefhorst et al. and Chisholm et al. showing that LXR activation leads to hepatic steatosis [11], [23], our data also show LXR activation significantly increased the expression of genes involved in lipogenesis, including srebp-1c, chrebp, acc1, fas and scd1 (Figure 3), leading to elevated blood triglyceride and aggravated hepatic steatosis. Here, MLXIPL is linked to fatty liver disease.