SLC27A5 and Hepatic fibrosis: This is consistent with a previous report of a child with a homozygous mutation in SLC2A75 who developed extensive fibrosis.[18] Although SLC27A5 expression was not reduced in the liver biopsy, over 85% of the unconjugated BAs were present in the plasma of this child, leading us to speculate that the deficiency of BAs conjugation may result in liver fibrosis.