Interestingly, cortical resections from patients with tuberous sclerosis and FCD type II also demonstrated higher expression levels of NR2C as compared with control fetal or adult samples (Lozovaya et al., 2014); in addition to this, patch-clamp recordings on these cortical resections demonstrated the contribution of NR2C to NMDA currents confirming the potential role of NR2C to epileptogenesis in mTORpathies. This evidence concerns the gene GRIN2C and tuberous sclerosis.