Taken together, these results are suggestive of distinct mutational processes compared with primary DIPGs: primary DIPGs originate within a particular early developmental timespan that is amenable to transformation with H3F3A and ACVR1 mutation [23], whereas radiation-associated DIPGs appear to arise as a result of radiation-induced DNA damage in established oncogenic drivers of primary adult GBM. The gene discussed is ACVR1; the disease is glioblastoma.