Investigations were made in PTX3/apolipoprotein E double knockout mice (ptx3/apoE-/-) The lack of PTX3 in animals with a genetic background making them susceptible to atherosclerosis resulted in larger areas of atherosclerotic lesions, greater accumulation of macrophages, higher expression of adhesion molecules, cytokines and chemokines in the vascular wall (19). This evidence concerns the gene APOE and atherosclerosis.