Epidemiological studies have shown that abnormal lipid metabolism mostly leads to the deposition of lipid particles in the intima of the arterial wall, which is also an indispensable pathogenesis of atherosclerosis; while rosuvastatin, a selective HMG-CoA reductase inhibitor, is able to increase the number of hepatic low-density lipoprotein (LDL) receptors on cell surface, promote the absorption and catabolism of LDL, inhibit the hepatic synthesis of LDL, and therefore reduce the total number of very low-density lipoprotein (VLDL) and LDL microparticles. The gene discussed is HMGCR; the disease is atherosclerosis.