Activation by synthetic ligands of liver X receptor (LXR) α (NR1H3) led to the suppression of gluconeogenesis in mouse hepatocytes by down-regulation of phosphoenolpyruvate carboxykinase (PCK1 or PEPCK) gene (Laffitte BA et al. 2003; Herzog B et al. 2007). Notably, both NR1H3 and NR1H2 have been shown to co-localize and interact with receptor-interacting protein 1 (NRIP1 or RIP140) (Jakobsson T et al. 2007; Herzog B et al. 2007). Indeed, depending on the gene, RIP140 can function both as a co-activator and co-repressor of NR1H2 or NR1H3. In the liver for instance, NRIP1 may activate NR1H3 (LXRα)-mediated transcription from lipogenic genes such as FASN and repress transcription of PCK1 gene to regulate metabolic pathways (Herzog B et al. 2007).