“…“Eraser” demethylases (e.g., FTO, ALKBH5, and ALKBH3) can remove the m6A modification, and the m6A residue can be recognized by “readers” (e.g., YTHDC1/2, YTHDF1/2/3, IGF2BP1/2/3, HNRNP, and eIF3) [ 23 ]. m6A plays important roles in mRNA stabilization, splicing, degradation, and translation efficiency via altering target gene expression [ 24 , 25 ], and its function has been explored in various biological processes, including stem cell differentiation [ 26 ], embryonic development [ 27 ], DNA damage [ 28 ], and tumor progression [ 23 ], among others. As an important m6A regulator enzyme, the methyltransferase, METTL3, can promote tumor progression by regulating downstream target genes in leukemia [ 29 ], colorectal cancer [ 30 , 31 ], bladder cancer [ 32 ], and gastric cancer [ 33 ]; however, the relationship between the m6A writer, METTL3, and VM formation remains unclear.…”