The ADP-ribosylation factor-like protein 4C (ARL4C, also known as ARL7) gene is transcribed to yield mRNA. Cholesterol-loading or treatment with the synthetic agonists of liver X-receptors alpha (LXRα, NR1H3) and beta (LXRβ, NR1H2), such as T0901317 or GW3965, signiﬁcantly induced the expression of ARL4C in murine RAW 264.7 and human THP1 macrophage cell lines (Hong C et al. 2011; Engel T et al. 2004; Sun D et al. 2012). Transcriptional studies of primary macrophages from single and double knockout NR1H2 or NR1H3 mice treated with LXR ligands GW3965 or T0901317 revealed that both receptors independently regulate ARL4C and induction was abolished only in the absence of both receptors (Hong C et al. 2011). Induction of ARL4C mRNA expression by NR1H2 or NR1H3 agonist was preserved in the presence of cycloheximide, indicating that new protein synthesis is not required for the effect of LXRs on ARL7. Similar regulation of ARL4C mRNA expression was observed in human peripheral blood-derived monocytes (Hong C et al. 2011). NR1H2 or NR1H3 stimulation of ARL4C has been shown to transport cholesterol to the membrane for the ATP-binding cassette transporter A1 (ABCA1)-associated cholesterol removal (Engel T et al. 2004). Overexpression of ARL4C in HeLa cells enhances APOA1-mediated cholesterol efflux (Engel T et al. 2004).