Whereas Ldlr−/−Apobec1−/− mice fed a western-type diet and injected with a control AAV8.null vector experienced a further 65% progression in atherosclerosis over 2 months compared with baseline mice, Ldlr−/−Apobec1−/− mice treated with AAV8.mLDLR realized an 87% regression of atherosclerotic lesions after 3 months compared to baseline mice. The gene discussed is LDLR; the disease is atherosclerosis.