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By integrating findings from animal models, clinical imaging, and molecular biology, this work elucidates how dysfunctions in GABAergic interneurons (e.g., PV+, SST+, VIP+), GABA signaling pathways, and associated genes collectively disrupt the E/I balance in the brain, leading to core ASD symptoms such as social communication deficits, repetitive behaviors, and sensory abnormalities

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