For example, in mouse models of Fragile X syndrome, the most common genetic cause of human autism, there is a significantly delayed developmental switch to GABAergic inhibition due to prolonged elevation in neuronal [Cl−]i due in part to decreased KCC2 expression (Lemonnier et al., 2013), and blockade of up-regulated NKCC1-mediated Cl− import in this context normalizes [Cl−]i, electrophysiological responses, and autistic-like behaviors in these mice (Tyzio et al., 2014), and improves autistic behaviors in humans (Lemonnier et al., 2012). The gene discussed is SLC12A5; the disease is autism.