Low-density lipoprotein and its receptor (LDL and LDLR, respectively) are both implicated in the pathogenesis of NAFLD; as such, the reduction of its central protein component, apolipoprotein B (ApoB), is investigated by ELISA to assess hepatocyte lipid-accumulating tendencies [50]. This evidence concerns the gene APOB and metabolic dysfunction-associated steatotic liver disease.