Statins are a diverse group of drugs, which share the ability to inhibit HMG CoA reductase and thereby the conversion of acetoacetyl CoA to mevalonate, the rate-limiting step in cholesterol biosynthesis. By inhibiting mevalonate production statins inhibit the pathway leading to the generation of farnesylpyrophosphate and geranylgeranyl pyrophosphate, two pyrophosphates that are critical for the induction of a variety of signal transduction pathways, which promote a cascade of events leading to endothelial dysfunction, inflammation, proliferation, apoptosis and other effects important for atherogenesis. Even though statins share a common mode of action they differ by several features like chemical structure, affinity towards HMG CoA reductase and their relative lipophilicity. These features translate into marked differences in LDL cholesterol lowering efficacy, pharmacokinetic properties and differences in lipophilicity associated with different tissue affinity and penetration. Rosuvastatin and atorvastatin produce the greatest percentage change in LDL cholesterol. Fluvastatin and pravastatin are less prone to drug interactions, because they are not metabolized through the CYP450 3A4 system. The hydrophilic pravastatin does not inhibit proliferation and migration of vascular smooth muscle cells. Data from clinical trials with statins suggest that the efficacy in LDL cholesterol lowering plays the overriding role in cardiovascular event reduction.