Hereto, we (1) investigated the bone marrow phenotype of HDL-deficient APOA1-knockout (KO) mice and normolipidemic wild-type controls, and (2) evaluated the effect of a potential change in bone marrow functionality on atherosclerosis susceptibility through a bone marrow transfer from the two types of mice into hypercholesterolemic LDL receptor KO mice. This evidence concerns the gene LDLR and atherosclerosis.