NEAT1 was predominantly highly expressed in the cerebral cortex and could regulate neuronal cell differentiation, proliferation, as well as the PI3K‐AKT‐mTOR signaling pathway.[2, 9] Furthermore, enrichment analysis verified that upregulated genes were enriched in the PI3K‐AKT pathway and other immune‐inflammation pathways.[9] These findings underscore the intrinsic tissue pathology associated with epileptic seizures in TSC and highlight the importance of NEAT1 and PI3K/AKT/mTOR pathway. This evidence concerns the gene AKT1 and tuberous sclerosis.