Subsequently, pre-miRNA was transported into the cytoplasm and cleaved by Dicer into mature miRNAs.[61] Intriguingly, Alarcón et al found that pri-miRNAs, methylated by METTL3, promote DGCR8 to recognize and bind the substrates with m6A modification instead of other secondary structures in transcripts, thus enhancing miRNA maturation.[60] This revealed a novel mechanism for m6A regulators in human cancers. The gene discussed is METTL3; the disease is cancer.