N6-methyladenosine RNA methylation is the most abundant modification in eukaryotic mRNA. It is catalyzed by the m6A-methyltransferase core complex, in which METTL3 serves as the catalytic subunit. This study investigated the effect of METTL3 activation on global RNA in diffuse large B-cell lymphoma, subtype activated B-cell. The U-2946 cell line was treated with METTL3 activator-1 and changes in gene expression and m6A levels were assessed using TRIzol-based RNA extraction, gel electrophoresis, m6A dot blotting, nanopore sequencing, and qPCR. Differential expression analysis using DESeq2 resulted in 41 significantly differentially expressed genes. Functional enrichment analysis revealed that affected genes were primarily involved in protein synthesis and translation, mitochondrial energy metabolism, and pathways related to nuclear export and nucleocytoplasmic transport. Notably, genes associated with DNA repair (XRCC3, RAD51B, SMC3) and apoptosis (CYCS) were downregulated, suggesting that METTL3 activation potentially induces genomic instability and avoidance of apoptosis, hallmarks of cancer. Genes involved in translation and RNA processing were dysregulated supporting the established role of METTL3 in regulating RNA metabolism. Comparison with the OncoKB curated gene list identified the differentially expressed genes SDHD and SMC3 as tumor suppressors. Collectively, these findings suggest that METTL3-mediated m6A regulation may contribute to the pathogenesis of diffuse large B-cell lymphoma.