In insulin-resistant states, insulin may lose its inhibitory control on hepatic glucose production but retain its direct stimulatory effect on DNL.2,3 This divergence in insulin sensitivity has been referred to as “selective hepatic insulin resistance” and has been suggested to drive the accumulation of liver fat, along with the increased circulating levels of glucose, insulin, and triglycerides associated with IR.3-5. This evidence concerns the gene INS and Insulin resistance.