Restenosis is the main problem after interventional therapy in lower extremity arteriosclerosis obliterans.Fatty acid-binding protein 4 (FABP4) is mainly secreted by macrophages and promotes lipid accumulation in macrophages, thereby converting macrophages into foam cells and causing atherosclerosis. After atherosclerotic occlusion interventional therapy, vascular endothelial cells can also specifically secrete FABP4; FABP4 acts on vascular smooth muscle cells, causing them to proliferate and migrate to form proliferative intima, and promote inflammatory response, resulting in restenosis after interventional therapy. It is suggested that FABP4 may be an important target for the treatment of atherosclerosis and restenosis after interventional therapy. This article briefly describes the biological characteristics and functions of FABP4, and reviews its role and mechanism in atherosclerosis and restenosis after interventional therapy.