To test this concept, we and others have investigated transgenic mouse lines with constitutive overexpression of the CRD-NRG1 isoform under control of the Thy1.2 or CamKII promoter and found several brain endophenotypes with relevance for schizophrenia, including ventricular enlargement, impaired prepulse inhibition (PPI), anxiety-like behavior, and deficits in working memory.14–16 Together, these studies imply hyperactive CRD-NRG1/ErbB4 signaling as an attractive candidate for a major signalopathy in schizophrenia. This evidence concerns the gene CAMK2G and schizophrenia.