Increased excitatory-inhibitory ratio is suggested to underlie the pathogenesis of autism and successful clinical trials have shown that the NKCC1 antagonist bumetanide, which restores low (Cl−)I and GABAergic inhibition, also attenuates the severity of autism (Rubenstein and Merzenich, 2003; Lemonnier and Ben-Ari, 2010; Tyzio et al., 2014; Lee et al., 2016; Uzunova et al., 2016; Lemonnier et al., 2017). The gene discussed is SLC12A2; the disease is autism.