Human genetic studies have shown that loss-of-function mutations in the EP300 gene, which encodes HAT P300, cause Rubinstein-Taybi syndrome, which is manifested as hypoplasia of the corpus callosum, congenital hypomyelination, and other systemic abnormalities48, suggested that P300 may serve as a vital regulator in OL development. This evidence concerns the gene EP300 and Rubinstein-Taybi syndrome.