Although we cannot provide a conclusion on how PTRF regulates TLR4 based on the present data, we provide indirect evidence that the high expression of both PTRF (in NAFLD) and TLR4 (in CIA) may be the contributing factor for the more severe phenotype of liver dysfunction in the compound NAFLD + CIA rats. This evidence concerns the gene TLR4 and metabolic dysfunction-associated steatotic liver disease.