GLYT2 deficiency, in contrast, is associated with hypertonia, ataxia, exaggerated startle responses called hyperekplexia, and early postnatal lethality; this is thought to reflect impaired reuptake of vesicular glycine into glycinergic neurons following glycine release (presynaptic recycling), leading to insufficient inhibitory activity3, 4. Here, SLC6A5 is linked to hyperekplexia.