In recent years, studies on m6A modification in tumors have been emerging, with a growing number of reports focusing on its role in HCC.[21] Classic m6A modifications are primarily conducted by “writers” such as METTL3/METTL14/WTAP or “erasers” like ALKBH5/FTO, modifying the m6A sites on targeted gene mRNA; “readers” such as IGF2BP1/2/3, YTHDF1/2/3 recognize and bind to the target gene mRNA for stabilization or degradation.[22] Our study discovered for the first time that ALKBH5 downregulated the m6A methylation level of TMCO3 mRNA, with IGF2BP2 participating in its mRNA stabilization. This evidence concerns the gene METTL14 and hepatocellular carcinoma.