Finally, we note that the severe hypercholesterolemia seen in the nr1h3−/− mutant animals fed the HCD provides a unique system for studying atherosclerosis: this degree of non-HDL cholesterol increase was achieved without additional genetic manipulations, reflecting conservation of aspects of lipoprotein metabolism other established models lack (Yin et al., 2012), such as the retention of an ortholog of the human Cholesteryl Ester Transfer Protein gene (Schlegel, 2016). Here, CETP is linked to familial hypercholesterolemia.