The neuropsychiatric disorder SCZ is a devastating mental disorder that impacts more than 21 million individuals globally (van Os & Kapur, 2009). SCZ was among the first neuropsychiatric disorders whose pathophysiology was modeled using patient derived iPS cells (Brennand et al., 2011; Chiang et al., 2011). These studies assayed connectivity, synapse number, spine density and expression of glutamatergic receptors in iPS cell derived neurons. Interestingly, application of the dopamine antagonist loxapine, but not other structurally similar antipsychotics, during the final three weeks of differentiation resulted in an elevation of neuronal connectivity in iPS-cell derived neurons from idiopathic SCZ patients. This suggests drug screening in SCZ human neurons can possibly identify specific compounds for its treatment. On the other hand, iPS cell disease modeling from SCZ subjects with defined genetic factors have also been established. For example, iPS cells with mutations in Disrupted in Schizophrenia 1 (DISC1), which encodes a protein involved in neurite outgrowth and cortical development (Wen et al., 2014; Ye et al., 2017), have been generated. Neurons derived from iPS cells harboring DISC1 mutations had synaptic defects, and
