Editorial: m6A methylation and cancer immunity

N 6 -methyladenosine (m 6 A) is the most prevalent and well-characterized internal RNA modification in eukaryotic cells. Acting at the post-transcriptional level, it regulates RNA splicing, export, stability, and translation, thereby maintaining cellular homeostasis and coordinating stress responses [1; 2]. The deposition and removal of m 6 A are controlled by three classes of enzymes including writers such as METTL3, METTL14, and WTAP, erasers such as FTO and ALKBH5, and readers such as YTHDFs and IGF2BPs, whose coordinated activity ensures precise regulation of RNA metabolism [3; 4; 5]. Recent evidence indicates that m 6 A functions not only as a key epitranscriptomic mechanism for cell differentiation and metabolic regulation but also as a central regulator of tumor immunity [6]. By modulating antigen presentation, interferon signaling, and immune cell differentiation, m 6 A shapes the tumor immune microenvironment (TIME) and determines immune evasion and responsiveness to immunotherapy [7; 8]. In innate immunity, m 6 A prevents the accumulation of endogenous double-stranded RNA, limiting aberrant interferon activation and maintaining immune balance, while in adaptive immunity it regulates the differentiation and effector functions of CD8⁺ T cells, dendritic cells, and tumor-associated macrophages, thereby influencing the formation of an immunosuppressive microenvironment and altering therapeutic sensitivity [9; 10]. Pharmacological inhibition of m 6 A methyltransferases induces double-stranded RNA accumulation and activates interferon signaling, which enhances antigen presentation and improves the efficacy of PD-1 blockade therapy [11]. Overall, m 6 A methylation represents a convergence point linking metabolic reprogramming, epitranscriptomic regulation, and immune microenvironment remodeling, serving as an essential integrator of tumorimmune interactions. In this context, Frontiers in Immunology introduces the Research Topic "m 6 A Methylation and Cancer Immunity", which highlights recent advances in m 6 A-mediated immune regulation and explores its mechanistic and translational implications for immune evasion, therapeutic response, and combination strategies. The following articles illustrate the latest progress in this rapidly evolving field.