Our extensive studies in the mutant GABAA receptor and GAT-1 suggest that impaired protein trafficking due to protein misfolding is a common aetiology in genetic epilepsy and neurodevelopmental disorders.10,11,15,16 This thus provides a great opportunity for treatment development by leveraging the protein trafficking pathway, via which the misfolded mutant protein is processed. Here, SLC6A1 is linked to neurodevelopmental disorder.