A notable convergence is upon NMDA receptor (NMDAR) signalling, providing a genetic complement to, and corroboration of, the prominent pre-existing hypothesis that NMDAR hypofunction (and glutamate synaptic function more generally) is important in the pathophysiology of schizophrenia (Coyle et al., 2003; Frohlich and Van Horn, 2014; Harrison and Eastwood, 1998; Kantrowitz and Javitt, 2010; Marek et al., 2010; Olney and Farber, 1995). The initial suggestions for a genetic convergence on NMDAR signalling were based on candidate gene findings (Collier and Li, 2003; Harrison and Owen, 2003; Harrison and Weinberger, 2005; Moghaddam, 2003) and received preliminary support from a bibliometric analysis (Harrison and West, 2006). Much stronger evidence has followed. NMDAR-related and postsynaptic signalling complex genes are over-represented amongst schizophrenia-associated CNVs (Kirov et al., 2012) and are also enriched for rare variants (Fromer et al., 2014; Purcell et al., 2014; Timms et al., 2013). Finally, a SNP within the NMDAR GRIN2A subunit gene is now genome-wide significant for schizophrenia, as are SNPs at the loci for GRIA1, GRM3 and SRR (Table 1), all of which impact on NMDAR signalling. Moreover, NMDAR
