However, knockdown of METTL14 had a higher incidence of tumorigenicity in glioblastoma stem cells (GSCs) than knockdown of METTL3 (Cui et al., 2017), suggesting that METTL14 may have other functions in addition to forming a heterodimer with METTL3 to install m6A. Recent studies suggest that METTL3 and METTL14 could be recruited to different genomic loci by various chromatin-binding proteins or histone modifiers. The gene discussed is METTL3; the disease is glioblastoma.