The proposed mechanisms include a high enrichment of Tmem108, a schizophrenia-susceptibility gene, in DG granule cells which results in impaired glutamatergic transmission in mice (Jiao et al., 2017), the reduction of glutamate signaling measured specifically in DG of schizophrenia patients (Stan et al., 2015), and alteration of adult hippocampal neurogenesis that was reported both in animal models and patients (Reif et al., 2006; Walton et al., 2012). This evidence concerns the gene TMEM108 and schizophrenia.