Although it is unknown whether GCL functions in muscle development, the catalytic subunit GCLC was reported to be activated by insulin through PI3K/Akt/mTOR/Nrf2/GCLC pathway upon hyperglycemia-induced stress in human brain endothelial cells, whereby attenuating the hyperglycemia-induced apoptosis via maintaining cellular redox balance [45]. The gene discussed is MTOR; the disease is Hyperglycemia.