A possible mechanism of action for these enzymes in the context of glioma progression was recently proposed by Li et al. The authors suggest that METTL3 is involved in decreasing nonsense-mediated mRNA decay (NMD) of transcripts encoding for splicing factors by m6A deposition around the start codon of serine and arginine rich splicing factor (SRSF) mRNAs. Here, METTL3 is linked to central nervous system cancer.