AKT1 and myasthenia gravis: In contrast, it has been shown that myoinhibitor gene deletion leads to a significant increase in Akt activity in ex vivo skeletal muscle, and that treatment of mice with monoclonal antibodies that block myoinhibitor (e.g., REGN1033) is effective in increasing muscle mass and strength and preventing further loss of muscle mass in models of myasthenia gravis that include braking and dexamethasone treatment [40].