Conversely, by stimulating adipose-specific lymphangiogenesis via VEGFR-3 to resolve metabolic syndrome in high-fat diet fed mice, Chakraborty et al. (2019) recently demonstrated that adipose-specific VEGF-D overexpression induced de novo lymphangiogenesis and these transgenic mice exhibited improved metabolic responsiveness and reduced obesity-associated macrophage accumulation as immune trafficking was increased from adipose tissue. This evidence concerns the gene VEGFD and obesity due to melanocortin 4 receptor deficiency.