Deletion of the fatty acid transporter CD36 in LECs results in attenuated VEGF-C-induced Akt activation, impaired cellular oxidative metabolism, junctional VE-cadherin destabilization development of leaky gut lymphatics, and obesity in mice, suggesting that intracellular VEGFR3 signaling may be an attractive target for translational studies [154]. The gene discussed is VEGFC; the disease is Obesity.