It has been shown that activation of TGR5 blunts the production of a cluster of differentiation 36 (CD36), scavenger receptor A (SR-A), monocyte chemoattractant protein-1 (MCP-1), and chemokine ligand-5 (CCL5) through the cAMP–NF-κB signaling pathway [79], which reduces the uptake of oxidized LDL (Ox-LDL) and the formation of foam cells, thereby inhibiting the progression of atherosclerosis. The gene discussed is CCL2; the disease is atherosclerosis.