Patients with MASLD frequently present with hyperlipidemia, and the metabolic dysfunction associated with MASLD can further exacerbate dyslipidemia.[18] Targeting pathways to reduce blood lipids, liver fat, and inflammation is a key approach to prevent and treat MASLD.[19] To establish a clinically relevant MASLD model, we fed male APOE(‐/‐) mice an HFHFHC diet for 12 weeks to induce liver lesions and hyperlipidemia.[20] Simultaneously, hepatic asprosin was overexpressed in HFHFHC‐fed mice via tail vein injection of an AAV8 plasmid (Figure 4a). Here, FBN1 is linked to metabolic dysfunction-associated steatotic liver disease.