Recent studies have elucidated a dual mechanistic role of VEGF-B in DKD: (1) MC-derived VEGF-B activates endothelial VEGFR1 through paracrine signaling, promoting fatty acid uptake and renal injury; (2) adipose tissue VEGF-B enhances lipolysis via hormone-sensitive lipase (HSL), increasing the number of circulating fatty acids that activate mesangial VEGF-B signaling, thereby establishing a pathological 'adipose-circulation-kidney' axis 147. The gene discussed is LIPE; the disease is diabetic kidney disease.