TMAO can change the bile acid spectrum to accelerate the formation of aortic lesions in ApoE−/− mice, and further activate the nuclear receptors farnesoid-X-receptor (FXR) and small heterodimer partner (SHP), to reduce the expression of cholesterol 7α-hydroxylase (Cyp7a1) to inhibit bile acid synthesis, thus accelerating the formation of atherosclerosis (82). This evidence concerns the gene NR1H4 and atherosclerosis.