Atherosclerosis is a result from the association of lipid deposition in the arterial wall and inflammatory process. This inflammatory process may be detected by clinical markers of systemic inflammation, such as ultrasensible C-reactive protein, which is associated with cardiovascular risk, independently of lipid levels. Statins reduce the inflammation associated to atherosclerosis, which may be verified by a reduction of the C-reactive protein levels. It seems that statins alter immune function by modulating post-translational protein prenylation. Individual genetic variations are associated with modulation of statins lipid-lowering effect; however, few studies have related the effect of the genetic variants with anti-inflammatory effect of statins. In addition to the genes involved in the cholesterol metabolism, genetic factors affecting statins pharmacodynamics and/or pharmacokinetics are potentially responsible for lipid and anti-inflammatory effects.