This study reports that a subset of obese people can preserve insulin-sensitivity, at least in the short-term, possibly by a mechanism that limits deposition of excess fat in the liver. This paper is significant because it highlights that it may not be appropriate to treat all obese people the same. It is becoming increasingly apparent that fat distribution, more than obesity per se, is a major risk factor for diabetes and cardiovascular disease. Excess ectopic-fat deposits in the abdominal region, liver and skeletal muscles have major metabolic consequences, leading to insulin resistance. The study by Stefan et al. supports the proposition that, despite having excess body fat, some obese people have a healthy metabolic profile that is equivalent to the profile in insulin-sensitive people in the normal weight range {1,2}. Stefan et al. found that insulin-sensitive obese people had reduced fat deposits in the liver and a reduced intima-media thickness of the coronary artery (an indirect measure of atherosclerosis development), compared with similarly obese, but insulin resistant, counterparts. Moreover, this insulin-sensitive obese group had a metabolic profile similar to the normal weight group. Do these ‘metabolically benign’ obese people represent a distinct phenotype or a short-term state on the continuum to insulin resistance if obesity persists? The percentages of liver fat in the normal weight, overweight and obese insulin-sensitive groups were not different (and all had significantly lower than the obese insulin-resistant group), which could suggest that accumulation of liver fat may be related to duration of exposure to insulin-resistance -- although the cause and effect relationship between insulin resistance and increased fat deposits in the liver remains unresolved {3}. Insulin-sensitivity is very responsive to decreases in weight loss {4}; thus, one could speculate that the greater insulin sensitivity in the obese insulin-sensitive group (relative to the overweight and the obese insulin-resistant groups) may be related to a recent loss of body mass that has normalized insulin-sensitivity; however, no information on recent weight changes was reported. This study does highlight the need for large-scale prospective studies to confirm and characterize this intriguing phenotype. If it is confirmed that a phenotypically distinct group of ‘metabolically benign’ obese people, who do not have increased mortality rates compared to normal weight people, does exist, this could have important implications with respect to obesity management and treatment.