The study conducted by Chakraborty et al. substantiated this possibility, demonstrating that an increased VEGFD-induced lymphangiogenesis in adipose tissue mitigated the obesity-related immune accumulation and increased the metabolism.244 Subsequently, they observed that VEGFD-induced lymphangiogenesis in adipose tissue resulted in a decrease in the macrophage populations and accelerated systemic fatty acid utilization, thereby facilitating the remodeling of the inflammatory response.245. The gene discussed is VEGFD; the disease is Obesity.