Focal gains in PDGFRA, EGFR, and VEGFR are seen in approximately 32% of DIPG cases, with PI3K alterations including constitutive activating mutations in PIK3CA, PIK3R1, and loss of function of PTEN (seen in 43% of patients combined), the latter associated with worse overall survival in DIPG (70). Here, PIK3CA is linked to diffuse intrinsic pontine glioma.