In an experimental NASH study, um-PEA supplementation upregulated the expression of PPAR-α and the phosphorylation level of adenosine monophosphate (AMP)-activated protein kinase (AMPK), while reducing the expression of acetyl-CoA carboxylase-1 (ACC1) and CD36 in hepatic cells[34]. The gene discussed is ACACA; the disease is metabolic dysfunction-associated steatohepatitis.