Noteworthy, recent findings highlighted that the expression of a truncated form of MeCP2, including just the MBD and the NID, rescues neurological phenotypes in Mecp2-deficient mice [29], thus suggesting that the primary function of MeCP2 is the recruitment of the NCoR/SMRT co-repressor complex to methylated DNA, and that alterations in this process are leading causes of RTT. The gene discussed is NID1; the disease is Rett syndrome.