Interestingly, METTL3 and IGF2BP2 are key members of the m6A methylation machinery, with METTL3 acting as a methylation writer and IGF2BP2 as a reader[30, 31] Dysregulated m6A methylation has been reported to play a significant role in the remodeling of the TME and promoting tumor metastasis.[32] In this study, in addition to the metastasis‐related pathways, we observed that additional immune‐related pathways were enriched through the pathway enrichment analysis of DEPs. Here, METTL3 is linked to neoplasm.