Overexpression of the AhR in the liver significantly upregulates the expression of the fatty acid translocase (FAT) CD36 in mouse liver cells, promoting the uptake of fatty acids by liver cells (Yao et al., 2016), which exacerbated lipid deposition in the liver, leading to liver damage and promoting the development of NAFLD. Here, CD36 is linked to metabolic dysfunction-associated steatotic liver disease.