Very similar glycinergic mIPSC features that we describe here for Slc7a10-null mice have been described for mice lacking the glycine transporter GLYT2, mutations in which are a known cause of hyperekplexia in humans; these parallels provide compelling support for the interpretation that the phenotype of Slc7a10-null mice represents hyperekplexia3, 15. The gene discussed is SLC6A5; the disease is hyperekplexia.