It has been suggested that dyslipidemia is abnormal in PBC without a concomitant increase in hepatic steatosis, which is attributed to fibroblast growth factor 19 (FGF19), which has enhanced expression in PBC patients, and FGF19 induces a decrease in mitochondrial acetyl coenzyme A carboxylase-2 (AAC2), which in turn promotes free fatty acid oxidation; inhibit insulin-related fatty acid synthesis in hepatocytes by suppressing the activity of sterol regulatory element binding protein 1C and elevated SHP expression [35], and reduce hepatic fat accumulation and plasma triglyceride levels. This evidence concerns the gene NR0B2 and metabolic syndrome.