However, this model has been extended by the existence of homomeric presynaptic GlyRs, which contribute to SD pathology; the presynaptic Asc-1 (alanine-serine-cysteine transporter 1), which is important for glycine and serine transport; the presence of extrasynaptic GlyRs, also coupled to gephyrin; and a possibly modulatory role of the interaction partner syndapin I in SD (Figs. 1 and 2, Table 1; Chapdelaine and others 2021; Langlhofer and others 2020; Safory and others 2015; Xiong and others 2014). This evidence concerns the gene SLC7A10 and Salla disease.