In addition, the blood glucose–lowering effect of PF-739 was diminished in mice deficient of AMPKα1 and AMPKα2 in skeletal muscle but not in liver, indicating that activation of AMPK in skeletal muscle is the appropriate means for the treatment of patients with type 2 diabetes independently of hepatic AMPK activation (161). The gene discussed is PRKAB1; the disease is type 2 diabetes mellitus.