MeCP2 mutations in the MBD or NID, which impair the formation of this bridge, are sufficient to cause RTT, and the expression of a radically truncated form of MeCP2, containing only MBD and NID, reverts neurological symptoms in Mecp2-null models [28,29,122], which underlines the importance of the MeCP2-mediated transcriptional repression for neuronal function. This evidence concerns the gene NID1 and Rett syndrome.