Cholesteryl ester transfer protein (CETP) transfers cholesteryl esters from high density lipoprotein particles to triglyceride-rich lipoproteins for subsequent clearance by the liver. CETP expression can be transcriptionally activated by liver X receptors (LXRα (NR1H3) and LXRβ (NR1H2)) that belong to the nuclear receptor superfamily of ligand-activated transcription factors. Activation of NR1H2,3 induced expression via an LXR response element (LXRE) consisting of 2 hexanucleotide sequences separated by 4 intervening bases (an LXRE of the DR4 type) in the CETP promoter (Luo Y & Tall AR 2000), which may be more responsive to NR1H3 (LXRα) rather than NR1H2 (LXRβ) (Honzumi S et al. 2010). Treatment with T0901317, a synthetic agonist of NR1H2, 3, increased CETP mRNA levels in human liver carcinoma HepG2 cells by approximately 220%, while NR1H3 silencing markedly diminished the increased expression of CETP (Shimada A et al. 2016). It should be noted that CETP is not expressed in the mouse or rat (it is a pseudogene in these species, Hogarth CA et al. 2003), so studies of LXR-mediated regulation of CETP and its effects have been performed in human, hamster, and non-human primates (Groot PHE, et al. 2005).