The shared genetic architecture underlying neuropsychiatric disorders implicates common molecular mechanisms.1 For example, while homozygous null mutations in CNTNAP2 lead to cortical dysplasia-focal epilepsy syndrome,2, 3 heterozygous intragenic deletions are associated with schizophrenia, intellectual disability, language deficits, seizures, and autism traits.4 Critically, CNTNAP2 variants are not completely penetrant.2, 5 Animal studies indicate a role for CNTNAP2 in axon guidance, dendritic arborization, and synaptogenesis.6–8. Here, CNTNAP2 is linked to cerebral cortical dysplasia.