In many animal experiments, bile acids, in addition to being a regulator of blood lipid and cholesterol content by participating in lipid metabolism, also act as signal molecules that activate different nuclear receptors, such as the farnesoid X receptor (FXR), pregnane X receptor (PXR), vitamin D receptor (VDR), and transmembrane G protein-coupled receptor 5 (TGR5), which reduce the risk of atherosclerosis via a variety of metabolic pathways in diverse tissues [15, 18, 33–35]. The gene discussed is NR1I2; the disease is atherosclerosis.