Existing studies have identified that nearly 90% of DIPG patients carry the histone H3 mutation H3K27M, and mutations in protein phosphatase, magnesium‐dependent 1, delta (PPM1D), tumor protein p53 (TP53), phosphatidylinositol‐4,5‐bisphosphate 3‐kinase, catalytic subunit alpha (PIK3CA), and activin A receptor type 1 (ACVR1) are also common.[5, 6, 7] These somatic hypermutations are closely related with the occurrence and development of DIPG, and therefore they are expected to become therapeutic targets for DIPG.[7] Our laboratory discovered the PPM1D mutation in DIPG for the first time. This evidence concerns the gene TP53 and diffuse intrinsic pontine glioma.