Nevertheless, Meechan et al.'s intriguing finding of abnormal interneuron migration due to reduced 22q11.2 gene dosage, particularly the Cxcr4 gene, suggests a molecular mechanism for disrupted neurodevelopment in 22q11DS, a possibility which should be investigated further in both animal models and human post-mortem studies. The gene discussed is CXCR4; the disease is 22q11.2 deletion syndrome.