Finally, we examined the properties of α2β and α2R323Lβ GlyRs using single-channel recordings (Figures 4–6), excluding the possibility that these mutant GlyRs resulted in spontaneously-opening channels, a known pathomechanism in startle disease involving GlyR α1β dysfunction (Chung et al., 2010; Bode et al., 2013; James et al., 2013; Zhang et al., 2016). This evidence concerns the gene GARS1 and hereditary hyperekplexia.