To investigate whether LRP1 regulates atherosclerosis through the PDGFRβ-dependent PI3K pathway in vivo, we generated a compound mutant mouse model by crossing smLRP1−/−; LDLR−/− mice to PI3K binding-deficient PDGFRβ F2/F2 mutant mice, in which tyrosine residues at position 739 and 750 are mutated to phenylalanines [18]. This evidence concerns the gene LDLR and atherosclerosis.