Several groups have generated heterogeneous neuronal populations from a variety patient derived hiPSCs, focusing either on genetically defined (Chiang et al., 2011; Pedrosa et al., 2011; Wen et al., 2014) or unknown genetic (Brennand et al., 2011, 2015) patient cohorts. Chiang et al. (2011) were the first to report hiPSCs lines from three SZ patients harboring DISC1 mutations, which have been long implicated in SZ and other neuropsychiatric disorders, including autism and major depression. Although this mutation is known to occur in only two rare family pedigrees, the DISC1 protein is thought to bind many proteins involved in neuronal development and synapse formation (Duan et al., 2007; Porteous et al., 2014), potentially providing broader insights into disease mechanisms. Wen et al. (2014) advanced this work by generating fore-brain like neurons from SZ patients with a DISC1 mutations as well as isogenic hiPSC lines, correcting mutations in one of the patients and introducing frameshift deletions in DISC1 into control hiPSCs. The corrected isogenic lines showed an improvement in synaptic functionality, as evidenced by the increase in synaptic markers (co-localization of SYN1
