In collaboration with the laboratory of Mauro Costa‐DiMatteoli at Baylor College of Medicine, the Noebels laboratory made the discovery that activation of the mechanistic Target of Rapamycin (mTOR) complex 2 (mTORC2), rather than mTORC1, is responsible for the antiepileptic effects of rapamycin therapy, and its reduction could represent a promising translational target for early brain disorders associated with IS where mTOR is dysregulated, such as tuberous sclerosis.36 This evidence concerns the gene MTOR and tuberous sclerosis.