LDLR and atherosclerosis: In summary, our present study reports for the first time that expressing human ApoL1 G2 per se in the livers of LDLR−/− hamsters has no detrimental effect on atherosclerotic development; however, hepatic ApoL1 G2 expression coordinates with a second hit, such as high fat intake to cause severe hyperlipidemia, to exacerbate diet-induced atherosclerosis accompanied with kidney and liver injury.