IntroductionrnCircular RNAs (circRNAs) are generated by the non-canonical back-splicing of pre-mRNA and have been shown to be present in a wide variety of tissues at lower expression levels than their asso-ciated linear RNAs1. The advent of high-throughput sequencing technologies has enabled the identification of circRNAs with bio-logical functions in diseases, particularly cancers. Because their stable circular structures resist digestion by RNase R, circRNAs accumulate in the brain with aging in a conservative form wherein neurons seldom undergo mitosis; some of these RNAs have been reported to serve as prognostic biomarkers for central nervous system (CNS) disease2. CircRNAs were initially believed not to be translated into proteins but to function as microRNA sponges or transcriptional regulators in cells. According to their origin of cyclization, circRNAs can be divided into 3 groups: exonic cir-cRNAs (EcRNAs), intronic RNAs (CiRNAs), and exon-intron circRNAs (EIcRNAs)3. CiRNAs and EIcRNAs usually exist in the nucleus, whereas EcRNAs are exported into the cytoplasm4. Recent studies on circRNAs have shown that some EcRNAs with a short open reading frame (sORF) might encode functional proteins through 5\'cap independent translation5. More novel proteins encoded by circRNAs have been demonstrated to play key roles in tumorigenesis, particularly that of glioblastoma mul-tiforme (GBM). Our team has previously explored the roles of circRNA-encoded proteins in GBM; here, we comprehensively summarize their regulatory effects in GBM.