Mutations in GluN2B have been linked to numerous types of epilepsy including epileptic encephalopathies, focal epilepsy, partial seizures, and infantile spasms.79–81 In addition, deletion of GluN2B leads to an increase in the number of excitatory inputs onto pyramidal neurons in the prefrontal cortex.64 In the current study, we also detected an increase in CA1 spine density in the absence of the GluN2B CTD and, in CA3, we found prolongation of epileptiform bursts in response to mGluR1/5 activation. The gene discussed is GRM1; the disease is infantile spasms.