Lp(a) functions as a dual pathogen that is thrombogenic, one through its LDL-like characteristics and the other through its plasminogen-like properties.49,50 It forms a link between genetics and two major explanations of the pathogenesis of atherosclerosis: the fibrin-deposition theory of Rokitansky and the lipid hypothesis of Virchow.51,52 Recently, it has been proposed that in settings of enhanced oxidative stress and elevated Lp(a) levels, a pro-inflammatory milie may predominate that contributes to the clinical expression of CAD.53,54. This evidence concerns the gene PLG and atherosclerosis.