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In addition to a key role of the mTORC2–Akt–FoxO pathway in the control of muscle homeostasis, deletion of the mTORC1 component Raptor in the skeletal muscle results in profound atrophic and dystrophic muscles, with metabolic and structural changes incompatible with mouse survival ( Tsc1 results in hypertrophy, sustained mTORC1 hyperactivation eventually precipitates atrophy in most muscles and premature death ( Atg7 in the skeletal muscle, where aberrant membranous structures accumulate in muscle fibers ( Tsc1 -KO (sm- Tsc1 KO) mice
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