Simple SummaryBrain tumours are a leading cause of cancer-related death in people under the age of 40, but most remain untreatable. There is an urgent need for a greater understanding of tumour biology to help guide the development of new treatments. We hypothesise that a type of genetic code—RNA—may be key to understanding how these tumours develop, and so how to treat them. Evidence has shown that the modification of this RNA is altered in brain tumours, and this may serve to regulate diverse mechanisms including tumour proliferation, invasion and treatment evasion. However, the precise mechanisms by which these RNA modifications exert their functional effects are poorly understood. This review summarises the evidence for this disordered regulation of RNA methylation in glioblastoma, and explores the downstream functional effects of such modification on RNA fate.AbstractGlioblastoma is the most prevalent primary brain tumour and invariably confers a poor prognosis. The immense intra-tumoral heterogeneity of glioblastoma and its ability to rapidly develop treatment resistance are key barriers to successful therapy. As such, there is an urgent need for the greater understanding of the tumour biology in order to guide the development of novel therapeutics in this field. N6-methyladenosine (m6A) is the most abundant of the RNA modifications in eukaryotes. Studies have demonstrated that the regulation of this RNA modification is altered in glioblastoma and may serve to regulate diverse mechanisms including glioma stem-cell self-renewal, tumorigenesis, invasion and treatment evasion. However, the precise mechanisms by which m6A modifications exert their functional effects are poorly understood. This review summarises the evidence for the disordered regulation of m6A in glioblastoma and discusses the downstream functional effects of m6A modification on RNA fate. The wide-ranging biological consequences of m6A modification raises the hope that novel cancer therapies can be targeted against this mechanism.