The myelination of axons is essential for neuronal wiring and normal nervous system functions. In the peripheral nervous system, Schwann cells (SCs) form myelin sheaths around axons during nerve development. Such myelination is compromised in a number of diseases. Hence, identification and understanding of the key pathways regulating SC development and myelinogenesis are essential for therapeutic progress. Here we uncover two separate roles of the cellular signaling node mTORC1 (mechanistic target of rapamycin complex 1) for regulating the development of SCs and subsequently the growth of myelin sheaths. Moreover, we demonstrate that defective SCs possess a remarkable plasticity to remyelinate axons via mTORC1. Thus, manipulating mTORC1 activity in diseased SCs could be therapeutically beneficial.