In a series of elegant studies, Matsuzaka et al. reported that mice deficient in Elovl6, the gene encoding the elongase that catalyzes the conversion of palmitate to stearate, were markedly protected against insulin resistance despite the fact that they could nevertheless become obese and develop hepatosteatosis when fed a high-fat diet. Because the liver plays an important role in regulating glucose tolerance and insulin resistance and because this organ is also metabolically sensitive to fat accumulation, these results provide evidence that either the process of fatty acid elongation or the ratio of C16 to C18 lipids might play a role in regulating liver insulin sensitivity. Though it is premature to identify Elovl6 as a therapeutic target for improving insulin resistance and preventing diabetes or cardiovascular disease risk, the metabolic fate of dietary fat could have important metabolic implications for modulating risk of type 2 diabetes and, possibly, cardiovascular disease.