The putative role of AKR1D1 in this regard is almost entirely unexplored; a single study found an association between increased systemic 5β-reductase activity and hepatic steatosis [16], another demonstrated decreased hepatic 5β-reductase expression in diabetic patients [17], whilst a third study reported elevated levels of 7-alpha-hydroxy-4-cholesten-3-one, the bile acid precursor substrate for AKR1D1, in patients with NAFLD [18]. The gene discussed is AKR1D1; the disease is fatty liver disease.