For simplicity, we highlight three features that would be relevant to an obesity adaptation: (1) interactions with the anti-VEGF drug Aflibercept, which could be directly used to model anti-VEGF therapy in obesity; (2) VEGF:soluble VEGFR1 binding, which sequesters VEGF from interacting with membrane VEGFRs, could downregulate membrane VEGFR activation and subsequent angiogenesis/adipogenesis in adipose tissue. The gene discussed is FLT1; the disease is obesity due to melanocortin 4 receptor deficiency.