Natural and synthetic ligands of liver X receptors (LXRα, NR1H3 and LXRβ, NR1H2) induced expression of a cluster of apolipoprotein genes APOE, APOC1, APOC2 and APOC4 in both human and mouse macrophages (Mak PA et al. 2002). The induction of all four mRNAs was greatly attenuated in peritoneal macrophages derived from LXR α/β-/- mice (Mak PA et al. 2002). Cell reporter assays suggest that the LXR response elements (LXRE) in the multienhancer regions ME.1 and ME.2, which confer tissue-specific expression in macrophages and adipocytes (Shih SJ et al. 2000), are necessary for the expression of this gene cluster (Mak PA et al. 2002). These secreted apolipoproteins regulate lipid transport and catabolism. APOC2 is recognized as an activator of lipoprotein lipase (reviewed in Wolska A et al. 2017). Thus the genetic deficiency of APOC2 results in a phenotype that resembles lipoprotein lipase deficiency, and is aptly called hyperlipoproteinemia type IB. Individuals lacking APOC2 exhibit hyperchylomicronemia and hypertriglyceridemia (reviewed in Wolska A et al. 2017).