The translational relevance of this LPAR2-regulated glutamatergic transmission was revealed by a human loss-of-function mutation of PRG1 (PRG1-R345T) [3], which results in cortical hyperexcitability and impaired somatosensory filter functions, specifically pre-pulse inhibition, a classical test in rodent models of schizophrenia and in clinical diagnosis of schizophrenia [5]. This evidence concerns the gene LPAR2 and schizophrenia.