The majority of cloned animals derived by nuclear transfer die during gestation and display neonatal abnormalities. However, because of the long generation interval of cloned animal species, the long-term consequences of cloning on health have been difficult to access. Recent studies in mice have provided evidence that cloned animals might have chronic health problems such as obesity. Obesity in cloned mice is likely to reflect epigenetic abnormalities that arise partly from inadequate nuclear programming; these obese mice display a unique phenotype that is suggestive of a defect other than malfunction of the leptin-melanocortin system, which occurs in most rodent models of obesity and in human obesity.