of our SCZD hiPSC neurons, many others, including ZNF804A, GABRB1, ERBB4, DISC1 and PDE4B, were aberrantly expressed in some but not all patients. Our data support the “watershed model”23 of SCZD whereby many different combinations of gene misfunction may disrupt the key pathways affected in SCZD. We predict that, as the number of SCZD cases studied using hiPSC neurons increases, a diminishing number of genes will be consistently affected across the growing patient cohort; instead, evidence will accumulate that a handful of essential pathways can be disrupted in diverse ways to result in SCZD.
