Moreover, even if many studies into GABA-mediated mechanisms in FXS indicate a reduction in both GABA-A and GABA-B activation in Fmr1-KO mice43–45, and in embryonic stem cell-derived human FXS neurons46, GABA-A and GABA-B agonists that have been tried in clinical trials, failed in reducing cortical hyperexcitability47. The gene discussed is FMR1; the disease is fragile X syndrome.