Alternatively, fluid accumulation in the K14-VEGFR-3-Ig mice, which expresses a soluble VEGFR-3-Ig construct in the skin under the keratin 14 promoter to trap VEGF-C/D, led to increased hydraulic conductivity to compensate for changes in interstitial fluid pressure, thus highlighting important pathological and functional differences although the lymphedema phenotype is similar in both strains (Rutkowski et al., 2010). This evidence concerns the gene KRT14 and lymphedema.