“…This modification arises postnatally due to high levels of DNMT3A, which persist throughout adulthood (Feng et al, 2005;Stroud et al, 2017). The discovery that MeCP2 targets mCAC sites preferentially over all other forms of mCH (Gabel et al, 2015;Lagger et al, 2017;Liu et al, 2018;Sperlazza et al, 2017) raised the possibility that this DNA binding specificity contributes to neuronal function. Non-CG methylation almost doubles the number of available MeCP2 binding sites in neurons (Lagger et al, 2017;Lister et al, 2013;Mo et al, 2015) and the timing of increased CAC methylation coincides with the increase in neuronal MeCP2 protein levels during the first few weeks of life (Guo et al, 2014;Lister et al, 2013;Skene et al, 2010;Stroud et al, 2017).…”