Integrated genomic, epigenomic and transcriptomic studies have provided insightful understanding of the tumorigenesis of pediatric DIPG, which also might hold promise for future utilization of molecular marker-driven clinical trials and use of novel targeted therapies such as HDAC, JMJD3, ACVR1, PPM1D, and BET bromodomain inhibitors, and CDK7 blockade40–44. This evidence concerns the gene ACVR1 and diffuse intrinsic pontine glioma.