Hypercholesterolemia, inflammation, and multiple growth factors, including VEGF-A/VEGFR-2 and FGF-2/FGFR-1 but not PDGF-BB/PDGFR-β might act synergistically to promote the development of immature and inflammatory intraplaque neovessels, and to accelerate the progression and instability of AS plaques in rabbits. This evidence concerns the gene KDR and familial hypercholesterolemia.