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. Here, SLC27A5 is linked to fibrosis.