Likewise, K14-VEGFR3-Ig mice in which a soluble form of extracellular VEGFR3 (sVEGFR3) that traps VEGF-C and VEGF-D was expressed from keratinocytes, were also resistant to high fat diet induced obesity, hepatic lipid accumulation and metabolic dysfunction (Karaman et al., 2015). This evidence concerns the gene VEGFD and obesity due to melanocortin 4 receptor deficiency.