In the different mouse models of MAFLD, activation of PPAR-α/β/δ induces catalase (CAT), promotes the conversion of FFAs to triglycerides to alleviate lipid toxicity, inhibits the generation of mt-ROS and the secretion of IL-1 and TNF in the lipid peroxidation reaction caused by excessive fat accumulation in mitochondria, and finally reduces the occurrence of liver fibrosis and MASH [104,105,106]. This evidence concerns the gene PPARA and metabolic dysfunction-associated steatohepatitis.