GlyT1‐ and GlyT2‐mutant mice also show early postnatal lethality associated with impaired glycinergic transmission and phenotypes mimicking human glycine encephalopathy and hyperekplexia (Gomeza et al, 2003a; Gomeza et al, 2003c; Eulenburg et al, 2010). Here, SLC6A5 is linked to glycine encephalopathy.