Abstract: Non-mutational epigenetic reprogramming and resistance to programmed cell death are key characteristics of tumors. N⁶-methyladenosine (m⁶A) is the most abundant post-transcriptional epigenetic modification in vivo. It plays important roles in apoptosis, autophagy, pyroptosis, necroptosis, andiron (Fe)-induced (ferroptosis) and copper (Cu)-induced (cuproptosis) death of tumor cells by targeting and regulating the key factors of programmed cell death. Epigenetic modulators targeting aberrant DNA methylation and histone modification are being used in clinical applications; however, drugs specifically targeting m⁶A modification regulation remain to be explored. In this review, the mechanisms of m⁶A modification regulating tumor cell programmed death is discussed with the aim of providing a theoretical basis for mediating tumor cell death by regulating the level of m⁶A modification as a potential tumor therapeutic strategy.