Cases have been reported to occasionally arise from pre‐existing pleomorphic xanthoastrocytomas (PXA) with the BRAF V600E mutation.[63] pTERT mutations are common in Ep‐GBM as well, along with CDKN2A homozygous deletion and PDGFRA amplification.[32] Although these molecular features have been identified to characterize Ep‐GBM, the challenge remains that their existence is irregular and probabilistic, leading to difficulties in targeting unified molecules to improve the survival of most patients with Ep‐GBM. The gene discussed is CDKN2A; the disease is glioblastoma.