In one study, mice reconstituted with LPLAT12-deficient hematopoietic cells developed more severe atherosclerotic lesions in the Ldlr-KO atherosclerosis model (171), while the other studies did not detect appreciable roles of LPLAT12 in macrophages or hematopoietic cells on atherosclerotic lesion formation in the same genetic atherosclerosis model (172, 173). This evidence concerns the gene LPCAT3 and atherosclerosis.