16p11.2 deletion is associated with hyperactivation of human iPSC-derived dopaminergic neuron networks and is rescued by RHOA inhibition in vitro.

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Researchers used stem cell technology to grow dopamine-producing brain cells from people with the 16p11.2 deletion and duplication, finding that deletion cells were overactive and larger than normal, while a drug called Rhosin was able to calm that overactivity—suggesting a potential treatment target for families affected by the deletion.