In this study, we performed a global and unbiased transcriptome analysis of iPSC-derived neurons from SZ and SAD patients with 22q11.2 deletion in comparison with neurons from healthy individuals (without the deletion). We reasoned that molecular changes would be easier to uncover from 22q11.2 deletion patients with SZ than other genetic subgroups, as 22q11.2 deletion is the most common known genetic risk factor and is associated with a very high penetrance, and the results could shed light on the molecular abnormalities and gene network disruption (due to combinatory effects of some 22q11.2 genes and candidates genes outside the region) in SZ developing brains. In addition to the two-fold reduction in the expression of genes that map to the 22q11.2 deleted region, our results showed altered expression of genes involved in apoptosis, cell cycle and survival, and MAPK signaling. These results are consistent with a number of previous reports showing abnormal apoptotic function in the neurodevelopmental and neurodegenerative processes associated with SZ [31–33]. Moreover, our analysis suggested that there might be an inter-chromosomal interaction between the 22q11.2 region and the HLA
