Recent studies on humans have emphasized this concept showing that even severe genetic mutations involving the insulin receptor resulted in hyperglycemia, hyperinsulinemia, ovulatory dysfunction, hyperandrogenism, acanthosis nigricans, and soft tissue overgrowth, but did not show manifestations of impairment of other insulin functions, presenting normal triglycerides, HDL- cholesterol, absence of liver steatosis, and adiponectin within the physiological limits. The gene discussed is INS; the disease is fatty liver disease.