In obese and insulin-resistant mice, VEGF-B gene transfer promoted weight loss and attenuated metabolic complications.22 In rats, VEGF-B also decreased coronary lipoprotein lipase activity and cardiac lipid metabolite accumulation and augmented cardiac insulin action, suggesting that it may be cardioprotective in diabetes.23 However, in long-term experiments, transgenic mice expressing only the human VEGF-B167 isoform in cardiomyocytes showed an increased death rate, apparently because of mitochondrial lipotoxicity.24 The gene discussed is VEGFB; the disease is diabetes mellitus.