As there is evidence supporting either enhanced or reduced NRG1 signaling in schizophrenia, no clear picture has emerged as to whether human NRG1 disease involves hypofunction or hyperfunction and this has led to the creation of distinct mouse models with opposing types of alterations in NRG1-ERBB signaling (Hashimoto et al., 2004; Petryshen et al., 2005; Hahn et al., 2006; Bertram et al., 2007; Parlapani et al., 2010; Shibuya et al., 2010). This evidence concerns the gene NRG1 and schizophrenia.