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. This evidence concerns the gene PHLDA1 and atherosclerosis.