Ideally, lipid-modifying drug therapy would lower low-density lipoprotein (LDL-C) and raise high-density lipoprotein (HDL-C).The key to the metabolic process of LDL-C and HDL-C is the transport and reversal of cholesterol.LDL-C transports cholesterol into the cell through the CD36 molecule on the membrane of macrophages in the vascular wall.ApoA1 transports free cholesterol from peripheral tissues through the membrane of macrophages in plaques via adenosine triphosphate Transport by adhesive clamp transport (ABCA1/ABCG1) transports free cholesterol from peripheral tissues; lecithin cholesterol acyltransferase esterifies free cholesterol to form nascent HDL particles, which gradually form large, mature HDL particles; HDL transports cholesterol esters to the liver, where they are transported back to hepatocytes for degradation and metabolism via scavenger receptor-B1 (SR-B1). Statins increase circulating HDL-C levels by promoting hepatic Apo-A1 and PPAR- synthesis; (thiazolidinediones, niacin and other lipid-modifying drugs). Therefore, in the process of atherosclerosis formation, there is both the transport of cholesterol into the vessel wall by LDL-C and the reverse cholesterol transport within the vessel wall. Lipid-modifying drugs, through their synergistic effects on Apo-A1, HDL, ABCA1 and ABCG1, and SR-B1, reduce the inflow of cholesterol and increase the outflow of cholesterol to achieve reverse cholesterol transport and cause AS plaque regression. Moderate lipid regulation means that statin therapy can achieve the target value of reducing cholesterol inflow into plaque: lowering LDL-C by more than 45% (1.81~2.42mmol/L), while achieving the target value of increasing cholesterol outflow from plaque: raising HDL-C by more than 8% (1.17~1.42mmol/L), which can achieve the regression of coronary plaque. The target value of lipid modulation for coronary plaque regression by statin therapy is not the use of high-dose statin.