Epsins, a family of adaptor proteins involved in clathrin-dependent endocytosis, control VEGFR-3 degradation in LECs for regulating lymphangiogenesis, lymphatic maturation and valve formation [134, 135], designing molecules to target increased expression of macrophage epsins may represent a therapeutic strategy to treat atherosclerosis [15]. The gene discussed is FLT4; the disease is atherosclerosis.