Prior work linking HCFC1 mutations to GABAergic deficits in mice [10] and radial glial abnormalities in zebrafish [9,14] suggest a multifaceted mechanism, wherein mTOR may underlie neurodevelopmental phenotypes and potentially intractable epilepsy in cblX syndrome and other HCFC1-related seizure disorders. This evidence concerns the gene MTOR and epilepsy.