AKT1 and muscle atrophy: Muscle atrophy, while not homogeneous in its etiology or pathophysiology, is recognized to reflect predominantly a shift in balance between protein synthesis and degradation, principally driven by the interaction of the anabolic insulin-like growth factor-1 (IGF-1)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway and the catabolic transcription factor forkhead box O (FoxO) and atrogenes (such as MuRF1 and MAFbx; refs. 2, 3).