Future work using CRISPR technology to evaluate patient-specific mutations such as that identified in the proband [15] will be used to improve our understanding of how metabolic function and fatty acid β-oxidation contribute to normal neural networking and whether deficiencies in CPT2 are likely to cause dysregulated gene expression associated with neurological disorders such as seizure and dopaminergic disease states such as schizophrenia. This evidence concerns the gene CPT2 and nervous system disorder.