HTG and NASH have been reported to be positively associated with the incidence of atherosclerosis 23; however, surprisingly, inactivation of ApoA5 had no effect on spontaneous atherosclerosis in both 8-month old and 18-month old hamsters on chow diet, but only mild atherosclerotic lesions were observed in HFD fed animals (Figure S3), indicating that NAFLD, rather than atherosclerotic cardiovascular disease (ASCVD), was the major event in the setting of ApoA5 deficiency in our hamster model. Here, APOA5 is linked to metabolic dysfunction-associated steatotic liver disease.