The study identifies that the N6-methyladenosine (m6A) modification marks primary microRNAs (pri-miRNAs) for processing by the microprocessor complex, which includes the RNA-binding protein DGCR8 and the ribonuclease DROSHA. The methyltransferase METTL3 is responsible for methylating pri-miRNAs, marking them for recognition and processing by DGCR8. METTL3 depletion reduces DGCR8 binding to pri-miRNAs and leads to a global decrease in mature miRNAs and an accumulation of unprocessed pri-miRNAs. In vitro processing experiments confirm that the m6A mark is sufficient to promote pri-miRNA processing. Gain-of-function experiments show that METTL3 enhances miRNA maturation in a global and non-cell-type specific manner. The study also reveals that the m6A modification is enriched in pri-miRNA sequences, as shown by m6A-seq and HITS-CLIP experiments. METTL3 depletion reduces the levels of methylated RNA bound by DGCR8, indicating a direct role of METTL3 in pri-miRNA processing. The m6A modification facilitates the recognition of pri-miRNA sequences by DGCR8, allowing for their processing into pre-miRNAs and mature miRNAs. The study further demonstrates that the m6A modification is conserved across vertebrates and plays a key role in the nucleus by enabling the microprocessor complex to recognize specific substrates. Altered METTL3 expression in human malignancies may contribute to aberrant miRNA expression in cancer. The findings highlight the importance of the m6A modification in the initiation of miRNA biogenesis and its role in regulating miRNA processing.The study identifies that the N6-methyladenosine (m6A) modification marks primary microRNAs (pri-miRNAs) for processing by the microprocessor complex, which includes the RNA-binding protein DGCR8 and the ribonuclease DROSHA. The methyltransferase METTL3 is responsible for methylating pri-miRNAs, marking them for recognition and processing by DGCR8. METTL3 depletion reduces DGCR8 binding to pri-miRNAs and leads to a global decrease in mature miRNAs and an accumulation of unprocessed pri-miRNAs. In vitro processing experiments confirm that the m6A mark is sufficient to promote pri-miRNA processing. Gain-of-function experiments show that METTL3 enhances miRNA maturation in a global and non-cell-type specific manner. The study also reveals that the m6A modification is enriched in pri-miRNA sequences, as shown by m6A-seq and HITS-CLIP experiments. METTL3 depletion reduces the levels of methylated RNA bound by DGCR8, indicating a direct role of METTL3 in pri-miRNA processing. The m6A modification facilitates the recognition of pri-miRNA sequences by DGCR8, allowing for their processing into pre-miRNAs and mature miRNAs. The study further demonstrates that the m6A modification is conserved across vertebrates and plays a key role in the nucleus by enabling the microprocessor complex to recognize specific substrates. Altered METTL3 expression in human malignancies may contribute to aberrant miRNA expression in cancer. The findings highlight the importance of the m6A modification in the initiation of miRNA biogenesis and its role in regulating miRNA processing.