Moreover, our results point out that the excessive lipid accumulation observed in livers of mice under IH conditions is likely due to the upregulation of CD36, which is involved in FFA uptake into hepatocytes, along with that of genes implicated in de novo lipogenesis, thus leading to the onset of hepatosteatosis, the earliest phase of NAFLD. This evidence concerns the gene CD36 and metabolic dysfunction-associated steatotic liver disease.