In case of RTS, glutamatergic hyperfunction seems to play an important role, too, since treatment of mice deficient for the 5mC-binding transcription factor Mecp2 with the mGluR5 negative allosteric modulator CPET and the NMDAR antagonist ketamine reduces RTS-associated phenotypes such as deficits in cognition and information processing, respectively [17, 18]. The gene discussed is MECP2; the disease is Rett syndrome.