More recently, FXR activation via FGF15 has been identified as a way to improve outcomes after brain-dead (BD) donor LT of steatotic and non-steatotic grafts in rats and indeed, BD induced intestinal damage and down-regulation of FXR and the resulting reduction in intestinal FGF15 was associated with low hepatic FGF15 levels, liver damage and regenerative failure. This evidence concerns the gene NR1H4 and Behcet disease.