In summary, by integrating information obtained from manifold analyses of reprogrammed neuronal cells, we deepened an in vitro mechanistic understanding of how the 22q11.2 microdeletion affects neurodevelopment. From the current results, we propose a hypothetical concept of ‘reduced neurogenic and elevated gliogenic competences' as a shared underpinning of etiologically heterogeneous schizophrenia. We also propose the potential benefit of developing compounds that have high specificity against p38α and can pass through blood–brain barrier, as novel therapeutics for schizophrenia.
