Prefrontal interneurons are derived from progenitors located in the ganglionic eminences of fetal forebrain.[46] From GD14 to GD18, interneurons migrated tangentially from ganglionic eminences to fetal forebrain cortex.[18, 30] Several studies indicated that interneuron migration retardation could induce autism‐like behaviors.[20, 21] In this current study, we further analyzed the influence of gestational 1‐NP exposure on GAD67+ interneurons in fetal mPFC and forebrain. The gene discussed is GAD1; the disease is autism.