In this report, we investigated whether loss of TDAG51 alters the development and progression of atherosclerosis by crossing TDAG51−/− mice20 with ApoE−/− mice, an established hyperlipidemic mouse model of accelerated atherosclerosis.21 Our findings provide the first in vivo evidence that deficiency of TDAG51 reduces atherosclerotic lesion growth. Here, APOE is linked to atherosclerosis.