During the occurrence and development of various types of cancer， oncogenes and surrounding regulatory regions can detach from chromosomes and form extrachromosomal DNA （ecDNA）. Because it is non-chromosomal inheritance， ecDNA drives high copy numbers of oncogenes and genetic heterogeneity within tumors， endowing tumors with the ability to quickly change their genomes， accelerating tumor evolution， and contributing to treatment resistance. In addition， the circular topology of ecDNA enhances chromatin accessibility， alters gene regulation and oncogene transcription， driving tumor growth and progression. The unequal separation of ecDNA from parent tumor cells to offspring cells rapidly increases the heterogeneity of tumors， providing them with adaptability to immunosuppressive microenvironment and drug therapy， and possibly providing an advantage in tumor evolution. Glioblastoma （GBM） is the most common and malignant neurological tumor， and the study of ecDNA in the field of gliomas is still in its initial stages. This article discusses the impact of ecDNA on the occurrence， development， and treatment resistance of GBM， highlights new research and proposes future research directions for GBM treatment targeting ecDNA， broadens understanding of GBM diseases， and helps to develop new diagnostic biomarkers and treatment targets for GBM from the perspective of ecDNA in the future.