Schizophrenia (SCZ) is a debilitating neuropsychiatric disorder with a strong developmental component, numerous perturbations in synaptic and network functions, and a polygenic risk profile (Adriano et al., 2012; Schizophrenia Working Group of the Psychiatric Genomics Consortium, 2014). One of the earliest studies of SCZ used hiPSCs derived neurons from a genetically heterogenous cohort of four SCZ patients and performed gene expression profiling, extensive characterization of neurite outgrowth and synaptic connectivity, as well as pharmacological treatment with antipsychotics (Brennand et al., 2011). SCZ patient cells differentially expressed 596 unique genes and showed deficits in synaptic connectivity, compared to controls, which were partially ameliorated by the antipsychotic drug Loxapine (Brennand et al., 2011). Furthermore, several groups investigated 22q11.2 hemizygous microdeletion, one of the few single loci associated with a large increase in risk for SCZ (see Bassett and Chow, 2008), in hiPSC derived cells. Neurospheres derived from the 22q11.2 deletion patients were smaller in size, had reduced expression levels of markers for cellular proliferation and survival, and an increased astrocyte to neuron ratio, consistent with observations in postmortem brains (Toyoshima et al.,
