Consistent with these findings, schizophrenia-like deficits and impaired maturation of glutamatergic synapses have also been described for mice deficient in Nrg1, ErbB4 and BACE1, a protease that initiates Nrg1 processing by cleaving its extracellular domain (Chen et al., 2008; Barros et al., 2009; Del Pino et al., 2013). Here, BACE1 is linked to schizophrenia.