The complexity of insulin action, which uses a variety of mechanisms, including post-transcriptional regulation, and is itself modulated both by allosteric regulation of responsible enzymes and by the availability of substrates for lipogenesis and gluconeogenesis, means that further study will be needed to understand the causal relationship between hepatic steatosis insulin resistance and fructose metabolism in the liver and kidney. The gene discussed is INS; the disease is Insulin resistance.