To ascertain whether overexpression of RAB39B participates in XLID, we injected AAVs overexpressing RAB39B or AAV‐EGFP (as a control) into bilateral ventricles of neonatal C57BL/6 wild‐type mice, carried out behavioural tests at 2 months of age and acquired brain tissues for further analysis at 3 months of age (Figure 1A,B). The gene discussed is RAB39B; the disease is cask-related x-linked intellectual disability.