Similarly, in the treatment of NAFLD, emodin can also increase mitochondrial fatty acid β-oxidation by mediating AMPK activation to reduce hepatic lipid accumulation, the molecular mechanism involves the improvement of IR in the PI3K/AKT2/AMPKα pathway and the promotion of gene expression of PPARα, CPT-1a and ACOX1 related to fatty acid oxidation (Tzeng et al., 2012b; Yu L. et al., 2020). The gene discussed is PPARA; the disease is metabolic dysfunction-associated steatotic liver disease.