Several copy number variations (CNVs) have been associated with increased SZ risk, including 22q11.2, 15q11.2, and NRXN1 loci (for review see St Clair, 2009). HiPSC studies of 22q11.2 deletions, found in approximately 1% of SZ cases (Bassett and Chow, 2008), have identified differential gene expression in pathways regulating cell cycle and development (Lin et al., 2016) as well as impaired neurite outgrowth and cellular migration (Toyoshima et al., 2016). Investigation of patient hiPSCs with a 15q11.2 microdeletion revealed deficits in apical polarity and adherens junctions due to CYFIP1 haploinsufficiency; genetic association analyses on these hiPSCs uncovered an epistatic interaction between a WAVE signaling mediator (involved in cytoskeleton development) and CYFIP1 (Yoon et al., 2014). Finally, NRXN1 expression was reduced in human embryonic stem cells (hESCs) by heterozygous deletion (Pak et al., 2015) and hiPSCs by shRNA (Zeng et al., 2013). Heterozygous mutant neurexins resulted in impaired neurotransmitter release and elevation of CASK (synaptic scaffolding protein) (Pak et al., 2015), and half reduction in NRXN1 expression led to changes in gene expression of cell adhesion and neuron differentiation pathways (Zeng et
