In the absence of age-matched healthy controls, we can only postulate that the vehicle-treated 34-day old SCZ cerebral organoids suffered a faster decrease in the CCO activity and E–I ratio when compared to healthy controls, possibly due to excitotoxic cell death37—see Fig. 2B and C. Here, energy supply from mitochondria is essential and can be limiting for synaptic activity during neurodevelopment in schizophrenia, which may reciprocally modulate the motility and fusion/fission balance of mitochondria in the dendrites22 as well as homeostatic plasticity64. This evidence concerns the gene RYR1 and schizophrenia.