can lead to ASD-like features. It remains unclear whether the deficiency of MeCP2 in these excitatory or inhibitory neurons disrupts the same circuits. Using mice engineered with a stop codon surrounded by loxP sites crossed with a ubiquitously-expressed inducible Cre line (CAG-Cre/Esr1), researchers have provided evidence that Rett syndrome phenotypes can be induced in fully developed mice (McGraw et al., 2011) and rescued through gene reactivation (Guy et al., 2007; Robinson et al., 2012; Lang et al., 2014), suggesting that ASDs may arise from persistent abnormal neural functioning, rather than disrupted development. However, this hypothesis needs to be tested in other models of ASD, as the phenotypes reported in these studies are not necessarily generalizable.
