The recent finding that MeCP2 binds to mCH at genes that are misregulated in Mecp2 knockout brains, and that mCH deposition occurs predominantly after birth in conjunction with neuronal maturation, has led to the hypothesis that failure of mutant MeCP2 to bind to mCH could account for the postnatal onset of RTT symptoms (Chen et al., 2015). The gene discussed is PMCH; the disease is Rett syndrome.