The disrupted intricate balance of bile acid synthesis (via cholesterol 7α-hydroxylase (CYP7A1)) transport (ABCG5/8/B11 and SLC10A1) and signaling pathways (primarily regulated by the farnesoid X receptor (FXR) and the liver X receptor (LXR)—key nuclear receptors that govern bile acid metabolism) contributes to the progression of hepatic steatosis and inflammation [134,135,136]. This evidence concerns the gene NR1H4 and fatty liver disease.