Serum amyloid A (SAA), including SAA1, SAA2 and SAA3, are acute response proteins, mainly produced by hepatocytes and regulated by inflammation-associated cytokines, which promote endothelial dysfunction via a pro-inflammatory and pro-thrombotic effect and were detected to be significantly elevated in Fah-deficient livers under NTBC treatment. Here, FAH is linked to endothelial dysfunction.