Our goal was to test, whether increased PDGFRβ signaling through PI3K is the primary cause for the increased susceptibility to atherosclerotic lesion development in LDLR −/− mice lacking LRP1 in their SMCs, and whether PDGFRβ-dependent PI3K signaling is required for the expression of the Marfan syndrome-like phenotype in smLRP1-deficient mice. This evidence concerns the gene LRP1 and Marfan syndrome.