Glioblastoma is an aggressive primary brain tumour in adults and has no significant improvement in survival rate so far.46 Previous studies strongly indicated the role of m6A methylation in self‐renewal and tumorigenesis of glioblastoma stem cells (GSCs).47 Reduction in m6A level induced by METTL3 silencing led to the up‐regulation of a group of oncogenes such as ADAM19, EPHA3 and KLF4, but a down‐regulation of tumour suppressors including CDKN2A, BRCA2 and TP53I11. The gene discussed is BRCA2; the disease is glioblastoma.