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With the advent of next-generation sequencing, the genetic landscape of childhood epilepsy is continuously evolving and currently comprises a wide range of genes, many of which are associated with the mechanistic target of rapamycin (mTOR) pathway. Recently, the relationship between hyperactivation of the mTOR signalling pathway and development of epilepsy has been widely recognized [1–3]. GTPase-activating protein (GAP) activity towards the RAG 1 (GATOR1) complex, a super-repressor of mTORC1, inactivates Rag proteins by altering their nucleotide loading status (GTP or GDP) and causes lysosomes to release mTORC1 [2].