Apolipoprotein L1 (ApoL1), coded by ApoL1 gene that is only expressed in humans, gorillas, and green monkeys, is largely synthesized by the liver and incorporated into high-density lipoprotein (HDL), playing beneficial roles in inflammation and Trypanosoma brucei infection.1 To date, except for the neutral allele of ApoL1 G0 which is a major form discovered in humans, two human ApoL1 alleles have been identified, including ApoL1 G1 and ApoL1 G2, which are highly associated with various human kidney diseases in the population-based studies.2 Over the past two decades, the relationship between ApoL1 risk alleles and atherosclerotic cardiovascular disease remains largely unexplored. Different transgenic murine models expressing human ApoL1 risk alleles have been constructed; however, they are widely used to investigate the impact of ApoL1 on kidney diseases but not atherosclerosis because wild-type mice with overnutrient intervention are still resistant to atherosclerosis.3 Recently, emerging evidence shows that Syrian golden hamsters lacking low-density lipoprotein receptor (LDLR−/−) replicate familial hypercholesterolemia, providing an ideal animal tool for studying human atherosclerosis.4