Atherogenesis is a complex process involving several cell types, including endothelial cells, platelets, and smooth muscle cells. The development of atherogenesis depends on the modification of the function of these cells due to the interaction of cellular receptors with a variety of peptide hormones as well as with lipoprotein particles. Appropriate treatment of risk factors for atherogenesis depends on this mechanism and must be individualized to fit the major mechanisms present in each patient. New tools are emerging to improve the ability to tailor risk management to fit the needs of particular patient subgroups.