GLYT1-deficiency leads to some, but not the full range, of the symptoms seen in glycine encephalopathy, an inherited human disease triggered by a primary defect in the glycine cleavage system that degrades excess of intracellular glycine, which leads to elevated levels of glycine in the blood and cerebrospinal fluid of the affected individuals (Gomeza et al., 2003; Kurolap et al., 2016). This evidence concerns the gene SLC6A9 and glycine encephalopathy.