Wenstedt et al. observed that salt-sensitive increases in blood pressure in individuals with Type 1 diabetes may be linked to the absence of macrophages and thus reduced lymphangiogenesis.252 Wu et al. demonstrated that diabetes-induced ROS-activated c-Src-dependent phosphorylation of VEGFR3 and upregulation of epsin expression, causing VEGFR3 degradation via the interaction between epsin and VEGFR3, ultimately leading to impaired lymphangiogenesis.253 In patients with Type 2 diabetes, increased lymphatic permeability has been demonstrated to lead to lymphatic vessel dysfunction. The gene discussed is FLT4; the disease is type 2 diabetes mellitus.