Abu-Hayyeh et al. have shown that levels of epiallopregnanolone sulphate—a sulphated progesterone metabolite—are above normal in patients with intrahepatic cholestasis of pregnancy. At these levels, epiallopregnanolone sulphate acted as a partial agonist for the farnesoid X receptor (FXR), mediating expression of bile acid homeostasis genes. Bile acid mediated recruitment of co-factor motifs to the FXR ligand binding domain was competitively inhibited by epiallopregnanolone sulphate.