The effects of CD59 deficiency were attenuated by administration of a blocking antibody to C5 in CD59−/− apoE−/− mice and targeted overexpression of human CD59 in endothelial and haemopoietic cells in apoE−/− mice resulted in resistance to the development of atherosclerosis, supporting a functional role for C5b-9 in the development and progression of atherosclerosis, plaque rupture, and thrombosis [110]. This evidence concerns the gene APOE and atherosclerosis.