METTL3 and neoplasm: Accumulating evidence indicates that m6A modifications are involved in the differentiation and functional regulatory network of MDSCs to create an inhibitory microenvironment conducive to tumor growth, including high METTL3 expression in cervical cancer and m6A modification-mediated Olfr29-ps1/miR-214-3p/MyD88 regulation in renal cancer [155, 156].