In GBM, high expression of methylated reader YTHDF2 recognizes METTL3‐mediated m6A modification, which activates the NF‐κB signaling pathway to promote the malignant progression of GBM.[5] In addition, recent studies reveal that CENPA, an m6A reader localized at centromeres, stabilizes m6A‐modified cenRNAs to ensure centromere integrity in cancer cells. Here, METTL3 is linked to glioblastoma.