N6-methyladenosine (m6A) is a prevalent internal modification on eukaryotic mRNA, primarily occurring in the RRACH sequence. It is installed by m6A methyltransferases and removed by m6A demethylases, with reader proteins recognizing and binding to m6A to regulate RNA metabolism. Alterations in m6A levels contribute to cancer pathogenesis by regulating the expression of tumor-related genes such as BRD4, MYC, SOCS2, and EGFR. This review discusses recent advances in the research of m6A enzymes, their underlying mechanisms in cancer pathogenesis and progression, and potential targets for cancer therapy. Key regulators of m6A include writers (METTL3, METTL14, WTAP, VIRMA, RBM15, ZC3H13, METTL16), erasers (FTO, ALKBH5), and readers (YTHDF1, YTHDF2, YTHDF3, YTHDC1, YTHDC2, IGF2BPs, EIF3, HNRNP A2B1). m6A functions as both a tumor promoter and a tumor suppressor, depending on the target gene and the balance between m6A levels and enzyme activity. Therapeutic strategies targeting m6A, such as selective inhibitors of FTO and ALKBH5, show promise in cancer treatment.N6-methyladenosine (m6A) is a prevalent internal modification on eukaryotic mRNA, primarily occurring in the RRACH sequence. It is installed by m6A methyltransferases and removed by m6A demethylases, with reader proteins recognizing and binding to m6A to regulate RNA metabolism. Alterations in m6A levels contribute to cancer pathogenesis by regulating the expression of tumor-related genes such as BRD4, MYC, SOCS2, and EGFR. This review discusses recent advances in the research of m6A enzymes, their underlying mechanisms in cancer pathogenesis and progression, and potential targets for cancer therapy. Key regulators of m6A include writers (METTL3, METTL14, WTAP, VIRMA, RBM15, ZC3H13, METTL16), erasers (FTO, ALKBH5), and readers (YTHDF1, YTHDF2, YTHDF3, YTHDC1, YTHDC2, IGF2BPs, EIF3, HNRNP A2B1). m6A functions as both a tumor promoter and a tumor suppressor, depending on the target gene and the balance between m6A levels and enzyme activity. Therapeutic strategies targeting m6A, such as selective inhibitors of FTO and ALKBH5, show promise in cancer treatment.