This thesis separated into two parts. The first part examined how the lack of GPAT affects atherosclerosis that depends on a western diet. The second part examined whether the lack of GPAT does ameliorates the atherosclerosis developing on an atherogenic diet. In the first part, we fed ApoE+/-/GPAT1-/- mice and ApoE+/- mice on western diet for 4 months. We found that ApoE+/-/GPAT1-/- mice and ApoE+/- mice did not develop atherosclerotic lesions after 4 months of western diet. ApoE+/-/GPAT1-/- mice had lower serum cholesterol, hepatic triacylglycerol and body weight than ApoE+/- mice. We could not conclude that ApoE+/-/GPAT1-/- mice could improve atherosclerosis. In the second experiment, we fed ApoE+/- and ApoE+/-/GPAT1-/-mice an atherogenic diet (15.8% fat, 1.25% cholesterol, 0.5% cholate) for 90 days. We wanted to see if ApoE+/-/GPAT1-/- mice improve the diet-induced atherosclerosis on these ApoE+/-mice. We found out the ApoE+/-/GPAT1-/- mice increased their serum cholesterol and VLDL-cholesterol compared to ApoE+/- mice. The atherosclerotic lesion sizes of ApoE+/-/GPAT1-/- mice and ApoE+/- mice were similar. We concluded that the absence of GPAT could not improve the diet-induced atherosclerosis.