Given that these previous findings observed in humans and mice demonstrated the paradoxical effects of ApoA5 on TG regulation and NAFLD, but mice partially or completely lacking ApoA5 only showed mildly or moderately elevated circulating TG concentration, which could not replicate HTG or sHTG in patients deficient with ApoA5, we applied CRISPR/Cas gene editing to target Apoa5 gene from Syrian golden hamster, a small rodent with metabolic features similar to humans. Here, APOA5 is linked to metabolic dysfunction-associated steatotic liver disease.