The macrophages that accumulate in atherosclerotic plaques efflux cholesterol to HDL particles via ABCA1 and ABCG1. Both transporters are regulated at the transcriptional level by LXRs and post-transcriptionally by miR-33. HDL particles exit the artery wall and return to the liver via the SR-BI receptor. In the liver, most cholesterol is transformed into bile acids and is secreted into the bile for excretion. Cholesterol esters (CE) from HDL can also be transferred to VLDL/LDL by the cholesterol ester transfer protein (CETP), and after that can be removed from the plasma through the hepatic LDL receptor (LDLr). In this issue of the JCI, Martel et al. suggest that lymphatic vessels play a key role in controlling HDL particle entry into and exit from atherosclerotic lesions, thereby regulating RCT. TG, triglycerides.