VEGFC and familial hypercholesterolemia: Furthermore, lymphangiogenesis is enhanced through treatment with VEGFC-156S (VEGF-C protein with a substitution of Cys156 by a serine residue), but reduced through VEGFR-3 inhibition, suggesting that hypercholesterolemia may trigger lymphangiogenesis in Apoe−/− mice through a mechanism dependent, in part, on VEGF-C [86].