For instance, a PV-neuron/Gad1 homozygous knockout mouse line (Georgiev et al, 2016) was spontaneously hyperactive but showed normal sensorimotor gating and spatial working memory, and had increased mRNAs for Pvalb, Bdnf, Kcns3 and Gad2. Since these mRNA are unaltered or decreased in patients with schizophrenia, it was suggested that PV neuron-selective GAD67 loss is not an upstream cause of schizophrenia (Georgiev et al, 2016). This evidence concerns the gene BDNF and schizophrenia.