Of note, it has been reported that also other pathways of CEC are impaired in FH subjects, such as SR-BI or ABCG1 cholesterol efflux31,36, as well as other steps of RCT including cholesterol ester exchanges between HDL and apoliprotein B-containing lipoproteins as well as hepatic HDL-C uptake31. Here, ABCG1 is linked to familial hyperaldosteronism.