The drug, bumetanide, which specifically antagonizes the NKCC1 chloride importer, has not only found favor in the treatment of some epilepsies, but has also been met with success in the treatment of symptoms of autism in early drug trials and is leading to exciting new developmental theories regarding the molecular pathology of autism (Dzhala et al., 2005; Ben-Ari et al., 2012; Lemonnier et al., 2012). This evidence concerns the gene SLC12A2 and epilepsy.