Another study verified that obesity- or hepatic steatosis induced UGT activity, steatosis was accompanied by increased hepatic triglyceride and free acid content and subsequently induced the network of transcriptional factors of aryl hydrocarbon receptor (AhR), constitutive androstane receptor (CAR), nuclear factor (erythroid-derived 2)-like 2 (Nrf2), pregnane Xreceptor (PXR), and peroxisome proliferator-activated receptor-α (PPAR-α) and then increased Ugt isoform mRNA expression. The gene discussed is PPARA; the disease is fatty liver disease.