type IV NRG1 (Law et al., 2006; Paterson et al., 2014; Tan et al., 2007), the CYT-1 isoform of ERBB4 (Law et al., 2007), and the p100δ isoform of the catalytic subunit of PI3K (Law et al., 2012). This isoform selectivity is not only pathophysiologically interesting, but may provide opportunities for selective drug targeting (Barrie et al., 2012; Lipscombe et al., 2013). Furthermore, NRG1 and ERBB4 have direct and indirect interactions with NMDAR signalling (Banerjee et al., 2010), whilst AKT1 (protein kinase C) impacts on the GSK3β–Wnt pathway which is also implicated in the disorder (Freyberg et al., 2010). These wider interactions highlight that there may be ‘meta-convergence’ of schizophrenia genetic risk across quasi-independent pathways.
