Studies have elegantly demonstrated this effect via the generation of smLRP1–/– mice on a background of LDLR deficiency, showing that smLRP1–/–/LDLR–/– mice are not only more susceptible to cholesterol-induced atherosclerosis than LDLR–/– mice but also exhibit PDGFR overexpression and increased phosphorylation of Smad2, a downstream component of the TGFβ pathway (14, 121). This evidence concerns the gene LDLR and atherosclerosis.