More recently, studies of humans with single gene disorders of proximal insulin signaling have supported the importance of partial insulin resistance: genetic defects in the insulin receptor, although replicating in severe form many features of common insulin resistance (hyperglycemia, extreme hyperinsulinemia, ovulatory dysfunction, hyperandrogenism, acanthosis nigricans, and soft tissue overgrowth), do not feature other critical components of the syndrome (elevated plasma triglycerides, suppressed HDL cholesterol, fatty liver [refs. 9, 10], and suppressed plasma adiponectin [ref. 11]). This evidence concerns the gene ADIPOQ and Hepatic steatosis.