We focused on astrocytes, as there is a direct correlation of astrocytic GAT-1 deficit with thalamic absence seizures.24,25 We first differentiated the iPSCs to NPCs and then differentiated the NPCs into astrocytes or inhibitory neurons as in our previous study.9 Human astrocytes derived from iPSCs around 30 days after differentiation were treated either with DMSO or with PBA (2 mM) for 24 h before the GABA uptake assay. The gene discussed is SLC6A1; the disease is Generalized non-motor (absence) seizure.