These inconsistencies have recently been reconciled in studies using a chronic, 30-week WTD model of NAFLD which suggested that PLIN2 in extra-hepatic tissues such as muscle and adipose mediates metabolic impairments associated with NAFLD, while hepatic PLIN2 specifically contributes to reduced hepatic steatosis, fibrosis, and immune cell infiltration [19]. Here, PLIN2 is linked to metabolic dysfunction-associated steatotic liver disease.