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An adequate and hopefully incisive therapeutic action will therefore depend on a finely orchestrated balance between the efficacy of the single treatment for the specific pathogenetic mechanism and the control of potentially noxious interactions among the different therapies

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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