It is still possible that microglia may be primary initiators of synaptic defects in other RTT models (Mecp2-/+, Mecp2 duplication, Mecp2R270X etc.), a mechanism recently reported in mouse models of frontotemporal dementia and Alzheimer's disease (Chahrour and Zoghbi, 2007; Chung et al., 2015; Baker et al., 2013; Chahrour et al., 2008; Hong et al., 2016; Lui et al., 2016). This evidence concerns the gene MECP2 and Alzheimer disease.