As a result, subsequent studies have suggested that alterations in either CDKL5 or FOXG1 should be classified as a distinct disorder from RTT as the majority of cases showed some differences in clinical features [11,12,13] Moreover, recent studies have suggested that RTT is a monogenic disorder caused by mutations that alter the functionality of the methyl-CpG-binding domain (MBD) and the NCoR/SMRT interaction domain (NID) in MECP2 [14,15,16]. Here, NCOR1 is linked to Rett syndrome.