In this review we have concentrated on the ways in which modification of LDL structure may account for foam cell formation. We have presented in vivo evidence as well as in vitro evidence supporting the proposition that modification of native LDL is a prerequisite for foam cell formation and atherogenesis. If further research supports the importance of LDL modification in atherogenesis, a whole new array of possibilities opens itself to us for intervention. At the moment, the only intervention that appears to be feasible is prevention of LDL oxidation; conceivably we might be able to interfere with the aggregation of LDL with itself or with other complexes in the artery wall that appear also to favor initiation of the atherogenic process.