The observation that increased inflammation associated with obesity is correlated with lymphatic dysfunction and reduced vessel density may seem contradictory provided that several studies have shown that under an inflammatory environment, lymphangiogenesis is stimulated as a mechanism for antigen clearance and inflammation resolution in response to pro-lymphangiogenic factors, such as VEGF-C, VEGF-D, and VEGF-A, that are secreted from infiltrating macrophages that respond to chemoattractants expressed by LECs (Kataru et al., 2009; Rahier et al., 2011; Kim et al., 2014). This evidence concerns the gene VEGFD and obesity due to melanocortin 4 receptor deficiency.