Using a mouse model expressing a human PRG-1 loss-of-function single-nucleotide polymorphism (SNP; PRG-1R346T), which leads to a dysregulated cortical information processing, and a well-established ketamine mouse model of schizophrenia [16], we could demonstrate the efficacy of pharmacological ATX inhibition in reducing hyperexcitatory cortical states and the associated characteristic schizophrenia-like phenotypes. Here, PLPPR4 is linked to schizophrenia.