This is consistent with the fact that although hepatic-specific knockdown of S6K enhances the ability of circulating hyperinsulinemia to lower glucose production in HFD rodents, basal glucose production during non-insulin-stimulated conditions did not alter in the HFD-hepatic-specific S6K knockdown vs. HFD-control rodents27. The gene discussed is RPS6KB1; the disease is hyperinsulinism.